Method of treating a pathological syndrome and a pharmaceutical agent

ABSTRACT

A method of treating a pathological syndrome includes administration of an activated form of ultra-low doses of antibodies to an antigen, wherein said activated form is obtained by repeated consecutive dilution combined with external impact, and the antigen is a substance or a pharmaceutical agent exerting influence upon the mechanisms of formation of this particular pathological syndrome. 
     Pharmaceutical agent for treating a pathological syndrome contains activated form of ultra-low doses of monoclonal, polyclonal or natural antibodies to an antigen, wherein said activated form is prepared by means of repeated consecutive dilution and external treatment, predominantly based on homeopathic technology, and said antigen is a substance or a drug acting as a direct cause of the pathological syndrome or involved in regulation of mechanisms of its formation. At that, activated forms of ultra-low doses of antibodies are raised against antigens of exogenous or endogenous origin, against autologous antigens, fetal antigens; anti-idiotypic antibodies are used too.

This application is a continuation of U.S. application Ser. No.11/656,226, filed Jan. 22, 2007, which is a continuation of U.S.application Ser. No. 10/311,666, filed Dec. 17, 2002, which is aNational Stage Application under 35 U.S.C. §371 of InternationalApplication No. PCT/RU01/00239, filed Jun. 19, 2001; which claims thebenefit of Russian Provisional Application Serial No. 2000115594, filedJun. 20, 2000.

FIELD OF THE INVENTION

The invention relates to medicine and can be employed for treatingvarious diseases and for producing pharmaceutical preparationspossessing no side effects.

DESCRIPTION OF THE BACKGROUND ART

The use of antibodies for treating pathological syndromes is well known(SU 1331508 A, A 61 K 39/00, 1984; SU 1730144 A1, C 12 N 7/00, 1992).

Also known are pharmaceutical preparations based on antibodies (serums,immunoglobulins) applied in therapeutic doses. (see, for example,Register of Pharmaceutical Agents of Russia, Encyclopedia of Drugs,7^(th) edition, 2000, pp. 358-359).

However, the range of application of these preparations is for the mostpart limited to etiological treatment of infectious diseases, and theiruse may be associated with undesirable side effects.

DESCRIPTION OF THE INVENTION

The invention is aimed at enhancing the efficacy of treatment ofpathological syndromes by the use of antibodies in activated forms forfundamentally new indications—to control a pathological syndrome; it isalso intended for producing pharmaceutical substances without markedside effects.

For solution of the given problem, the method for treating apathological syndrome includes administration of activated forms ofultra-low doses of antibodies to an antigen, wherein said activatedforms are obtained by repeated consecutive dilution combined withexternal treatment, and said antigen is a substance or a pharmaceuticalagent implicated in or exerting influence upon the mechanisms offormation of the pathological syndrome; said antigen can also representa substance (or drug) that is, upon its introduction into the body, withnon-medical purposes included, can act as direct cause of thepathological syndrome.

To this end it is expedient to use ultra-low doses of antibodies inactivated forms prepared by homeopathic technology of potentiation(dynamization).

Activated forms of ultra-low doses of antibodies to a substance or apharmaceutical agent can be also introduced together with this verysubstance or pharmaceutical agent implicated in or exerting influenceupon the mechanisms of the pathological syndrome or directly causing thepathological syndrome.

Besides, the objective is also accomplished by a pharmaceutical agentcontaining activated forms of ultra-low doses of monoclonal, polyclonalor natural antibodies to an antigen, wherein said activated forms areproduced by repeated consecutive dilution and external treatmentpredominantly based on homeopathic technology, and said antigen is asubstance or a pharmaceutical agent exerting influence upon regulationof the impaired function.

At that, antibodies used in activated (potentiated) forms of ultra-lowdoses are raised against antigens of exogenous or endogenous origin,against autologous antigens, fetal antigens; anti-idiotypic antibodiesare used too.

The drugs (pharmaceutical agents) obtained in accordance with thepresent invention constitute a novel class of pharmacologicalpreparations, distinctive in combination of specific pharmacologicalactivity, stable therapeutic action free from side effects, ecologicalpurity and low prime cost.

EMBODIMENTS OF THE INVENTION

The pharmaceutical preparation can be prepared in the following way.

1. Obtaining of Antibodies

Polyclonal antibodies specifically binding to compounds of variousclasses: proteins, polynucleotides, oligosaccharides, glycolipids, etc.and interacting with low-molecular substances (haptens) are obtainedthrough active immunization of animals. For this purpose, animals aregiven a series of antigen injections according to a specially designedpattern, the antigen being either an individually isolatedhigh-molecular substance, or a synthetic conjugate (for haptens). Thisprocedure results in obtaining a monospecific antiserum with highcontent of antibodies apt for further processing. If necessary theantibodies present in the antiserum are purified. Fractionating by saltprecipitation or ion exchange chromatography is used for this purpose.

Monoclonal antibodies of different specificity interacting both withlow-molecular haptens and with epitopes of high-molecular substances areobtained by means of hybridome technology. At that, the initial stage ofthe process includes immunization based on the principles alreadydeveloped for preparation of polyclonal antiserums. Further stages ofwork envisage yielding antibody-producing clones of hybrid cells,produced antibodies being of identical specificity. Their isolation iscarried out with the same methods as for polyclonal antiserums.

Natural antibodies to exogenous antigens and biological regulators ofvarious origins are isolated from human blood serum by the method ofaffinity chromatography. To this end, a carrier with a covalently boundantigen, either a hapten or a high-molecular compound is used as animmunosorbent. Chromatography yields antibodies with narrow specificityand affinity.

Methods of obtaining antibodies are described, for example, inImmunological Methods, under the editorship of G. Frimel, Moscow,Medicina Publishing House, 1987, p. 9-33).

Isolated antibodies to a substance or a pharmaceutical agent areconsecutively repeatedly diluted and exposed to external treatment untilultra-low or low doses are obtained, for example, in accordance withhomeopathic technology of potentiation (dynamization) (see V. Shvabe,Homeopathic Pharmaceutical Agents. A Manual on Description andPreparation, Moscow, 1967, p. 12-38). At that, the concentration isproportionally reduced through consecutive dilution of 1 volumetric partof the initial substance (antibodies) in 9 volumetric parts (for decimaldilutions, D) or in 99 volumetric parts (for centesimal dilutions, C) ofa neutral solvent until the required dose (potency) is obtained; eachdilution is followed by multiple vertical mechanical shaking; for eachdilution separate vessel is preferable.

External treatment in the process of dilution can also be performed bysound generator or other mechanical or electromagnetic action.

The pharmaceutical preparation thus yielded is used for the most part indosage forms and dilutions common for homeopathic practice, such asalcoholic or aqueous solutions or tablets (granules) obtained bysaturating the excipient of the formulation with potentiated solution orby direct introduction of the latter into liquid dosage form of thepreparation.

An example of obtaining a pharmaceutical preparation in form ofactivated polyclonal antibodies (antiserum) to morphine is given below.

1. Obtaining Morphine-Ovalbumin Conjugate.

Solution of 50 mg (0.001 mmol) ovalbumin in 5.0 ml of distilled waterwas mixed with 2.0 ml dimethylformamide containing 15.0 mg (0.039 mmol)of morphine 6-hemisuccinate and while the mixture was cooling thesolution of 15 mg (0.055 mmol) of water-soluble carbodiimide in 3 ml ofdistilled water was added to it by drops. The reaction mixture wasincubated for 5 hours at 4° C. The yielded conjugate was isolated by gelchromatography on Sephadex G25 column and exposed to lyophilization.

The quantity of conjugated morphine was calculated from UV-spectra ofthe original protein and the yielded conjugate by changes in absorptionat 280 nm. According to UV-spectra, the synthesized conjugate contained12-15 moles of hapten per mole of protein.

2. Obtaining a Monospecific Antiserum to Morphine-Ovalbumin Conjugate

Immunization of Viennese Blue rabbits weighing not more than 2 kg wasperformed in cycles with a 10-day interval between them. The maximalnumber of injections was four. The conjugate was injected into the areaof periarticular lymph nodes of front and hind paws in the dose of 1 mgper immunization. To this end the antigen was previously diluted in 1 mlof complete Freund's adjuvant. The total volume of immunization mixturewas 2 ml.

Subsequent immunizations were performed using incomplete Freund'sadjuvant, adhering to the above-mentioned proportions of antigen andadjuvant. A test blood sample was drawn from marginal ear vein of theanimal 10 days after immunization.

The rabbit blood serum was obtained by centrifugation at 1000 g for 10minutes at room temperature; after that chloroform was added as apreservative its final concentration reaching 13%.

The antiserum obtained was tested for specific antibodies to morphine bymeans of enzyme immunoassay, the antibodies being detected withconjugate of enzyme-labeled anti-species (anti-rabbit) antibodies.

The obtained antiserum contained specific antibodies active in thedilution 1:1000-1:25000.

Further on, γ-globulin fraction was isolated from the yielded antiserumTo this end the protein was precipitated with 50% ammonium sulfate withsubsequent rinsing of the precipitate with 30% saline solution,centrifugation and dialysis against phosphate buffer. The fraction thusprepared contained specific antibodies to morphine and was then used forproducing the pharmaceutical preparation.

3. Obtaining the Activated Form (Ultra-Low Dose) of the Antibodies toMorphine.

Antiserum γ-globulins (0.5 ml) was placed into E-61 vessel and mixedwith 4.5 ml of distilled water; the mixture was shaken 10 times yielding5 ml of the first centesimal dilution. The first centesimal dilution(0.05 ml) was placed into E-62 vessel with 4.95 ml of distilled water;the mixture was shaken 10 times yielding 5 ml of the second centesimaldilution. The centesimal dilutions from the third to the twenty-ninthwere prepared in a similar fashion. The thirtieth centesimal dilutionwas prepared by solving the twenty ninth one in 20% solution of ethanol.The yielded alcoholic solution was used for treatment purposes.

Examples of use of activated forms of ultra-low doses of antibodiesconventionally designated as potentiated (dynamized) antibodies (byanalogy with terminology used in homeopathic literature) for treatmentof various pathological syndromes are given below.

EXAMPLE 1 Potentiated Antibodies to Hypnotic Medications

A. Patient I., aged 46, a high school instructor, had long beensuffering from insomnia manifested by difficulties in falling asleep.The patient had a history of hepatitis (hepatitis and impairedmetabolism of xenobiotics in the liver resulting from it probablyaccounted for the aftereffects of the preparation). For the last sixmonths the patient had been taking 7.5 mg of IMOVAN at bedtime 2-3 timesa week; in the morning he suffered from drowsiness and dizziness. Thedose reduced to ½ tablet did not produce the desirable somniferouseffect. The treatment with antibodies to IMOVAN C200 in tablets wasstarted after discontinuation of IMOVAN intake. Two weeks laterdizziness and morning drowsiness disappeared. The patients sleep becamenormal.

B. Patient P., aged 62, complained of a sleeping disorder: awakening at2-3 a.m. The patient had been using barbiturate derivatives assomniferous medications but abandoned these drugs because of theirdecreasing efficiency. The patient was recommended to take 10 drops of a25% alcohol solution of potentiated monospecific antiserum to MIDAZOLAM(dormicum, flormidal,8-chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazo[1,5-a][1,4]benzodiazepinehydrochloride) at bedtime. Three days after the beginning of thetreatment the patient stated that he was easier falling asleep; thesleep duration extended to 7. A continued intake of the preparation wasrecommended.

C. Patient Ch., aged 42, was admitted to hospital in the condition ofmoderate alcohol intoxication. Next morning the patient complained oftremor and disorders in coordination of movements. After a single doseof 15 ml of an aqueous solution of potentiated monoclonal antibodies toNITRAZEPAM (radedorm,1,3-dihydro-7-nitro-5-phenyl-2H-1,4-benzodiazepine-2-one) C30 thepatient fell asleep. This suggested a conclusion that the preparationwas efficient in restoration of sleep in the process of arrestingalcohol abstinence syndrome.

D. Patient R., aged 48, a-driver by profession, presented complaints ofsleeping disorders due to overfatigue. An intranasal administration of0.5 ml of a potentiated aqueous solution C20 of antibodies to ZOLPIDEM(N,N,6-trimethyl-2-(4-methylphenyl)imidazolo[1,2-a]pyridine acetamide)at bedtime was suggested for controlling his insomnia: At a new visit 5days later the patient stated normalization of his sleep. Examinationdid not reveal any depression of reflexes or muscle tone. This suggesteda conclusion that this preparation can be prescribed to the patientswhose professional activities require precise coordination of movements.

E. Patient M., aged 54, complained of drowsiness and disorders incoordination of movements and presented a long-time history of the useof somniferous medications. After a 7-day course of treatment withpotentiated solution of monoclonal antibodies to ZOPICLON (imovan)(6-(5-chloro-2-pyridinyl)-6,7-dihydro-7-oxo-5H-pyrrolo-[3,4-b]-pyrazine-5-ylicester of 4-methyl-1-piperazine carboxylic acid) C50 in a dose of 1tablet twice a day the enhancement of motor activity and sleepnormalization were observed.

EXAMPLE 2 Potentiated Antibodies to Anesthetic Drugs

A. Patient M., aged 36, complained of nausea after the operation(appendectomy). For anesthesia THIOPENTAL SODIUM (monosodium salt of5-ethyldihydro-5-(1-methylbutyl)-2-thiooxo-4,6-(1H,5H)-pyrimidinedione)had been used. An oral intake of 20 ml of a C30 homeopathic dilution ofthe antiserum to thiopental 3 times a day was prescribed, which made itpossible to attenuate nausea.

B. Patient P., aged 28, complained of cramps in his lower extremitiesand hypertonicity of the gastrocnemius muscles. An oral intake of 15 mlof a C200 dilution of potentiated antiserum to SODIUM OXYBUTIRATE(sodium salt of 4-hydroxybenzoic acid) at bedtime was prescribed. Theexamination conducted 5 days later showed diminution of musculartonicity.

C. Patient M., aged 6, was admitted to the otorhinolaryngologic unit fora postoperative check-up after tonsillectomy. An oral administration ofa C30 solution of potentiated antibodies to KETAMINE[(++2-(2-chlorophenyl)-2-(methylamino)cyclohexanone hydrochloride] madeit possible to reduce the sensitivity of the child's mucosa and toperform an examination.

D. Patient A., aged 47, complained of hiccup and tachycardia afteradministration of ETHOMIDATE (ethyl ester of(R)-1-(1-phenylethyl)-1H-imidazole-5-carboxylic acid). A single oraldose of 50 ml of a homeopathic C30 solution of monoclonal antibodies toethomidate was administered. Thirty minutes later hiccup disappeared andthe cardiac rhythm was back to normal.

E. Patient D., aged 68, was admitted to a surgical hospital for ascheduled operation on benign prostatic hyperplasia. Three years earlierhe had undergone an operation for urolithiasis under HALOTHANE(1,1,1-trifluoro-2-chloro-2-bromoethane) anesthesia. The postoperativeperiod was complicated by liver function disorders manifested bydyspepsia, hyperbilirubinemia, and positive liver function tests. Thepatient presented a history of poor tolerance of other anesthetics.Therefore, slow intravenous infusion of 3 ml of potentiated antibodiesto HALOTHANE dissolved in a 5% glucose solution was used for anestheticpurposes. The operation and the postoperative period showed nocomplications.

EXAMPLE 3 Potentiated Antibodies to Anticonvulsant Drugs

A. Patient B., aged 19, has been suffering from generalized epilepsy(grand mal seizures combined with psychomotor symptoms) since the age of5. TEGRETOL (5-carbamoyl-5H-dibenz(b,f)azepine) chosen by thetrial-and-error method had proved to be the most efficientanticonvulsant drug for the patient; she had been receiving a dose of0.2 mg (1 tablet) 3 times a day for 2-years. The patients motherconsulted the attending doctor at to multiple bruises having appeared onthe patients body in the course of the last 10 days without anypreceding mechanical trauma. Total blood test revealed a depressed whiteblood (2.9×10³/μl) and platelet count (100×10³/μl). The treatment withC30 potentiated monoclonal antibodies to the dibenzoazepine groupforming the basis of the drug molecule was started whereas TEGRETOL wasdiscontinued. Two weeks later the blood pattern was back to normal, noepileptic seizures were registered.

EXAMPLE 4 Potentiated Antibodies to Antiparkinsonian Drugs

A. Patient Z., aged 37, developed parkinsonian symptoms after vernalencephalitis. The patient had been taking daily 10 mg (4 tablets) ofBROMOKRYPTINE (2-bromo-α-ergokryptine) with good effect but complainedof excessive fatigue, headaches, and constipation. The treatment withpotentiated antibodies to 2-bromo-α-ergokryptine (a C1000 dilution) in adaily dose of 1 tablet taken in the morning was started. Three weekslater the bowel function was back to normal and headaches subsided;however, complaints of excessive fatigue persisted.

B. Patient E., aged 72, was on LEVODOPA (3-hydroxy-1-tyrosine) forParkinson's disease. He complained of nausea and vomiting. Antiemeticdrugs of the phenothiazine group with smaller doses of LEVODOPA lead tothe exacerbation of his main disease. The use of a C200 dilution ofpolyclonal potentiated antibodies to LEVODOPA in a dose of 1 tablettwice a day improved the patient's tolerance to the preparation.

EXAMPLE 5 Potentiated Antibodies to Neuroleptics

A. Patient E., aged 42, was admitted to a psycho-neurological dispensaryin a condition of psychomotor agitation due to alcohol intoxication.Fifteen minutes after intravenous administration of 1 ml of a C30aqueous solution of potentiated antiserum to HALOPERIDOL(4-[4-(4-chlorophenyl)-4-hydroxy-1-piperidinyl]-1-(4-fluorophenyl)-1-butanonedecanoate) in a 5% glucose solution the agitation arrested and thepatient went to sleep.

B. Patient L., aged 50, consulted her physician for disorderedcoordination of movements. The examination revealed inhibited reflexesin her low extremities, namely the knee-jerk and the Achilles tendonreflexes. She presented a long-time (1.5 months) history of FLUPHENAZINE(moditene) intake. The discontinued use of the preparation was combinedwith an intranasal administration of a C30 aqueous solution ofmonoclonal antibodies to fluphenazine(4-[3-[2-(trifluoromethyl)-10H-phenothiazine-10-yl]propyl]-1-piperazinylethanol)and a once-a-day slow intravenous administration of a dose of 1 ml. Fourdays later the patients gait was back to normal and the muscle tone ofher low extremities increased.

C. Patient R., aged 62, complained of restlessness and groundless nightfears. Earlier she sought for physician's advice for insomnia and usedto take radedorm for it. Oral administration at bedtime of the antiserumto AZALEPTINE (clozapine, leponex)(8-chloro-11-(4-methyl-1-piperazinyl)-5H-dibenzo[b,e][1,4]diazepine) ina form of 10 ml of a C200 homeopathic solution was prescribed. Sevendays later phobias disappeared and the sleep became normal.

D. Patient Ch., aged 45, complained of tremor and disorderedcoordination of movements. He had a long-time history of neurolepticdrugs intake (haloperidol, aminazine) for schizophrenia. Oraladministration of 5 ml of a C30 dilution of homeopathic solution ofmonoclonal antibodies to RISPERIDONE(3-[2-[4-(6-fluoro-1,2-benzisoxazol-3-yl)piperidino]ethyl]-6,7,8,9-tetrahydro-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one)twice a day by intramuscular injections was prescribed. Repeatedexamination 7 days later revealed absence of tremor and a tendency tonormalization of the patients gait. No psychotic disorders wereobserved.

E. Patient S., aged 29, suffered from depressive-paranoid form ofschizophrenia. He had been taking neuroleptic drugs of the phenothiazineseries for some years; the best clinical effect was noted with TISERCINE(2-methoxy-10-(3-dimethylamino-2-methylpropyl)-phenothiazinehydrochloride). During last 4 months the patient himself and hisrelatives drew their attention to the aggravation of extrapyramidaldisorders and impaired bowel function (constipation). Total blood restrevealed depressed white blood count reaching the lower bound of normal(3.8×103/μl). The use of a C1000 dilution of potentiated monoclonalantibodies to PHENOTHIAZINE in a dose of 1 tablet 3 times a day for 20days (with discontinued tisercine intake) resulted in a markedrelaxation of extrapyramidal disorders and normalization of the bowelfunction; the patients white blood count increased to 4.7×103/μl. Nopsychotic disorders were present. The patients sleep, appetite and moodwere within normal limits.

F. Patient F., aged 19, suffered from oligophrenia in the form ofidiocy; aggressive behavior. She received a maintaining dose ofHALOPERIDOL(4-[4-(4-chlorophenyl)-4-hydroxy-1-piperidinyl]-1-(4-fluorophenyl)-1-butanonedecanoate) (20 mg daily) and displayed marked extrapyramidal disorders.The lowering of the dose resulted in the enhancement of the patientsaggressiveness. The use of a C30 dilution of polyclonal potentiatedantibodies to butyrophenone in a dose of 1 tablet twice a day improvedthe tolerance of HALOPERIDOL and made it possible to reduce the dose to5 mg a day and subsequently to maintain the patient in a satisfactorycondition by administering the potentiated preparation alone.

EXAMPLE 6 Potentiated Antibodies to Minor Tranquilizers

A. Patient V., aged 50, a research worker, has been receiving a daytimetranquilizer, MEZAPAM, for his obsessive-compulsive neurosis. Hecomplained of drowsiness (probably caused by impaired detoxifyingfunction of his liver). The use of a C30 dilution of potentiatedpolyclonal antibodies to the benzodiazepine nucleus made it possible toreplace the tranquilizer. The patient's condition became satisfactory;no neurotic disorders were noted.

B. Patient E., aged 71, complained of restlessness and insomnia. Oraladministration of a C200 preparation of potentiated polyclonalantibodies to DIAZEPAM(7-chloro-1,3-dihydro-1-methyl-5-phenyl-2H-1,4-benzodiazepine-2-one) ina dose of 1 tablet 3 times a day was prescribed. Four days later thedistrict physician noted normalization of sleep along with fewercomplaints of restlessness.

C. Patient S., aged 30, registered in a psycho-neurological dispensary,complained of the onset of restlessness, anxiety, and insomnia after thewithdrawal of PHENAZEPAM. Oral intake of the homeopathic solution ofantiserum to 2H-1,4-benzodiazepine twice a day was prescribed. After twodays of treatment the normalization of sleep and mood were noticed. Thegeneral state of health was satisfactory and no anxiety was observed.

D. Patient I., aged 39, complained of fatigability, disorders incoordination of movements, and restlessness. Examination revealed noorganic disorders of the central nervous system. After the diagnosis ofneurasthenia was established a course of treatment with a C12homeopathic solution of polyclonal anti-bodies to PHENIBUT(γ-amino-β-phenylbutyric acid hydrochloride) was suggested. After 2 daysof oral intake (1 tablet twice a day) of the preparation tremor subsidedand sleep became normal.

EXAMPLE 7 Potentiated Antibodies to Antidepressants

A. Patient V., aged 36, complained of the worsening of mood and sleepingdisorders in form of early awakening along with difficulties in fallingasleep. The patient also stated irritability and tremor withoutobjective reason. An intranasal administration of 5 drops of a C30homeopathic solution of antiserum to FLUOXETIN (PROZAC)(+−)-N-methyl-γ-[4-(trifluormethyl)phenoxy]benzolpropanamine) 3 times aday was recommended. Upon a new examination 5 days later the patientstated the betterment of his mood along with a tendency to normalizationof sleep. The physician's recommendation was to continue the course oftreatment.

B. Patient K., aged 39, complained of insomnia, tremor, restlessness,and impaired ability to work. He received a course of treatment with aC1000 dilution of potentiated polyclonal antibodies to FLUVOXAMINE((E)-5-methoxy-1-[4-(trifluormethyl)phenyl]-1-pentanone-O-(2-aminoethyl)oxime)in an oral dose of 1 tablet 4 times a day. After 3 days of regular drugintake the normalization of sleep was observed along with theimprovement of mood and control of restlessness.

C. Patient Sh., aged 56, complained of restlessness, feeling of fear,and sleep disorders. An intranasal administration of 1 ml of a 2% C30solution of antiserum to AMITRIPTYLINE(3-(10,11-dihydro-5H-dibenz[a,d]-cyclohepten-5-ylidene)-N,N-dimethyl-1-propanamine)3 times a day was recommended.

Upon a new examination 3 days later the patient stated the normalizationof sleep along with the reduction in the frequency and intensity of hisfits of phobia. He was advised to continue this treatment; high efficacyof the drug in this particular case was noted.

D. A young man aged 18 had been suffering from enuresis since hischildhood. AMITRIPTYLINE was found to have a good effect upon him. Afterthree weeks of treatment the patient's relatives noticed his drowsiness;the patient himself complained of visual disorders (impairedaccommodation) and bouts of arrhythmia from time to time. A C50 dilutionof potentiated monoclonal anti-bodies to the tricyclic group,constituting the nucleus of tricyclic antidepressants was prescribed ina dose of 1 tablet twice a day. The symptoms of side effects disappearedwhereas the curative action persisted.

E. Patient Ch., aged 32, a manager, presented a vast number ofcomplaints among which the dominating were constant tiredness, poorsleep with no refreshing effect, reduced ability to work, depression,constipation along with joint and muscle aches. This condition had beenlasting for more than half a year. A thorough clinical and laboratoryexamination revealed no psycho-neurological or somatic lesions thatwould account for such syndromes. The diagnosis of a chronic fatiguesyndrome was established. A month of combined therapy includingphysiotherapy, vitamin therapy, and antidepressant IMIPRAMINE intakeresulted in a mild positive effect. The treatment with a C200 dilutionof potentiated antibodies to IMIPRAMINE in a dose of 1 tablet 3 times aday was begun. A week later a marked improvement in the patient'scondition was noted; his ability to work increased and the number ofcomplaints declined.

F. Patient K., aged 29, was admitted to a psycho-neurological hospitalwith an established diagnosis of manic-depressive psychosis in the phaseof exacerbation. During examination the patient complained of the lackof motivations and tearfulness; the patient was not active physically.He used to take amitriptyline and diazepam for a long time. An oralintake of a C1000 solution of the antiserum to MOCLOBEMIDE (aurorix)(p-chloro-N-(2-morpholinoethyl)-benzamide) in the form of 5 ml of theaqueous solution 2 times a day was prescribed. A new examination 4 dayslater showed that the patient became more compliant; improved mood andenhanced liveliness were reported. A conclusion was drawn that thetherapy was efficient.

G. Patient C., aged 49, suffered from depression and sociophobia; he hadbeen receiving daily 225 mg of MOCLOBEMIDE (aurorix) (1.5 tablets inthree doses). Despite his attending-physician's warnings the patientsometimes broke his diet. Twice after eating a cheese sandwich and apizza with cheese he had episodes of hypertension, his blood pressurereaching 190/110 mm Hg. With moclobemide discontinued, a C30 dilution ofpotentiated polyclonal antibodies to moclobemide was administered in adose of 1 tablet once a day. Further on, the treatment was welltolerated and depression symptoms subsided rapidly.

H. Patient S., aged 44, developed fluctuations of mood, tearfulness, andlow vital activity caused by the climacteric period. Her psychiatristestimated these symptoms as manifestations of a depressive syndrome. Theuse of traditional antidepressants caused somnolence and lethargyinterfering with her professional duties. The prescription of a C12dilution of potentiated antiserum to CERTRALINE purified by affinitychromatography in a dose of 1 tablet twice a day resulted in a rapidimprovement of the patients general state and stabilization of her mood.

EXAMPLE 8 Potentiated Antibodies to Antiemetic Drugs of Central Action

A. Patient Zh., aged 64, developed nausea and vomiting during the courseof radio- and chemotherapy for peripheral lung cancer. The prescriptionof MOTILIUM controlled manifestations of dyspepsia but caused weakness,somnolence and intestinal cramps. With MOTILIUM discontinued, theadministration of 1 ml of a C6 dilution of potentiated antibodies toMOTILIUM in the form of intramuscular injections twice a day resulted inthe disappearance of neurotoxic and spastic reactions. The use of thepreparation was continued with a positive clinical effect.

EXAMPLE 9 Potentiated Antibodies to Central-Action Muscle Relaxants

A. Patient B., aged 25, developed contractures of his lower extremitiesafter a spinal trauma. MYDOCALM(1-piperidino-2-methyl-3-para-tolylpropanone-3 hydrochloride) in a doseof 300 mg a day was prescribed. After a favorable initial effect thepatient noticed a gradual increase in the muscular tension in his lowerextremities along with systemic arterial hypotension (105/60 mm Hg)after 2 months of the treatment. The prescription of a C200 dilution ofpotentiated antibodies to MYDOCALM in a dose of 1 tablet twice a dayresulted in the normalization of arterial blood pressure (120/70) aswell as in the reduction of muscular tension. The antibody therapy madeit possible to reduce the dose of MYDOCALM by 25%.

EXAMPLE 10 Potentiated Antibodies to Choline Esterase Inhibitors

A. Patient P., aged 20, with an established diagnosis of congenitalmyasthenia took UBRETIDE(3-oxy-1-methylpyridinium-hexamethylene-bis-(N-methylcarbamate)dibromide)(the maintaining dose was 1 tablet every other day). She startedcomplaining of excessive salivation and abdominal cramps. The use of aD6 dilution of potentiated antibodies to UBRETIDE in a daily morningdose of 1 tablet improved the patient's tolerance of UBRETIDE withoutreducing its efficacy and later made it possible to switch to therapywith the potentiated preparation only.

EXAMPLE 11 Potentiated Antibodies to Psychostimulants and NootropicDrugs

A. Patient M., aged 58, complained of memory disorders and insomnia. Anoral intake of 20 drops of an alcohol solution of antibodies toNOOTROPIL (pyracetam) (2-oxo-1-pyrrolidinylacetamide) in a potency ofC200 at bedtime was prescribed. During her second visit 7 days later thepatient reported of an extended duration of sleep along with lessdifficulties in falling asleep. The recommendation was to continue thecourse of treatment.

B. Patient M., aged 43, was admitted to hospital in the state of alcoholwithdrawal. The next day he started complaining of restlessness andtremor. A C30 dilution of potentiated antiserum to AMINALON (gammalon)(4-aminobutyric acid) in a dose of 1 tablet 6 times a day wasprescribed. The reduction of tremor and the improvement of mood werenoted. After 2 days of therapy the patient was discharged in asatisfactory condition.

C. Patient S., aged 72, complained of tachycardia and sleepingdisorders; she presented a long-time (3 weeks) history of SYDNOCARB(3-(α-methylphenyl)-N-phenyl-carbamoylsydnonimine) intake. Theintranasal administration of 10 drops of a C15 solution of monoclonalantibodies to SYDNOCARB 3 times a day was prescribed. An examinationafter 5 days of treatment revealed the absence of tachycardia; thepatient reported of less difficulties in falling asleep.

D. Patient V., aged 65, with an established diagnosis of asthenicsyndrome as a remote consequence of a cranio-cerebral trauma had beentaking MOLSIDOMINE (ethyl ester of N-carboxy-3-morpholino-sydnonimine)in a dose of 1 tablet 3 times a day (6 mg per diem) to prevent fits. Shesought her physician's advice for headaches and worsening of sleep.After MOLSIDOMINE withdrawal the treatment with C30 dilution ofpotentiated monoclonal antibodies to the sydnonimine group in a dose of1 tablet in the morning was started. The favorable effect of thetreatment has been lasting for 6 months.

E. Patient D., aged 38, complained of fatigability, weakness, andheadaches. The oral intake of 10 ml of a C40 dilution of potentiatedpolyclonal antibodies to CAFFEINE (1,3,7-trimethylxanthine) 3 times aday was prescribed. At his second visit to the physician 7 days laterthe patient pointed to easier awakening and the disappearance ofheadaches. He was recommended to continue the course of treatment.

F. Patient P., aged 35, a journalist by profession, presented symptomsof caffeine addiction: he had to drink up to 12-15 cups of strong coffeeto keep himself active. The patient was emotionally labile, inclined tooverestimating his own personality, and complained of poor sleep. Healso had a pronounced tremor of his hands. The use of a C200 dilution ofpotentiated antibodies to CAFFEINE (1,3,7-trimethylxanthine) in a doseof 1 tablet 3 times a day resulted in the reduction of the amount ofconsumed coffee to 4-5 cups, the improvement of sleep, the disappearanceof tremor, and better mood. Now the patient is active and manifests highworking efficiency.

G. Patient R., aged 78, is on regular treatment with PYRACETAM(nootropil) (2-oxo-1-pyrrolidinylacetamide) in a daily dose of 1.6 g forAlzheimer's disease. The general effect of the treatment beingfavorable, the patients relatives noticed enhancement of the patientssexual activity manifested by his inappropriate behavior. Thesubstitution of pyracetam by a C200 dilution of potentiated antibodiesto PYRACETAM made it possible to get rid of sexual disinhibition whilepreserving the nootropic effect.

H. Patient G., aged 4, suffered from mental retardation due to a birthtrauma. A 4-week course of everyday injections of CEREBROLYSINE (acomplex of peptides isolated from pig brain) resulted in someimprovement of the child's cognitive activity. During repeated coursesof treatment cerebrolysin was substituted by a C50 dilution ofpotentiated polyclonal antibodies to it (in a dose of 1 tablet 2 times aday). The patient's memory became much better as well as her abilitiesto develop and maintain skills.

EXAMPLE 12 Potentiated Antibodies to Preparations Improving CerebralCirculation

A. Patient L., aged 54, presented a history of cerebral atherosclerosisand an ischemic stroke a month ago. He was treated with HALIDOR(1-benzyl-1-(3-dimethylaminopropoxy)-cycloheptane fumarate) in tablets(100 mg twice a day). The patient complained of sleeping disorders andtachycardia (92 beats/min). The use of a C30 dilution of potentiatedantibodies to HALIDOR (in a daily dose of 1 tablet within a month)improved his sleep; his heart rate went down to 76-80 beats/min.

EXAMPLE 13 Potentiated Antibodies to Analeptic Drugs

A. Patient T. aged 15, was admitted in the state of alcoholintoxication. Examination revealed hypotension (90/60 mm Hg),bradycardia, and nausea. The intranasal administration of 1 ml per hourof a C200 dilution of antiserum to CORDIAMINE(N,N-diethyl-3-pyridinecarboxamide) was prescribed. After 6 hours of thetreatment nausea disappeared and the patients blood pressure was back tonormal.

EXAMPLE 14 Potentiated Antibodies to Anticonvulsant (Antiepileptic)Drugs

A. Patient D., aged 58, complained of tonic cramps in her lowerextremities.

The oral intake of calcium gluconate in combination with 10 ml of a D12homeopathic solution of antibodies to DEPAKIN (SODIUM VALPROATE) (sodium2-propylvalerate) at bedtime was recommended. The reduction ofconvulsive reactions was stated after 2 days of the therapy.

B. Patient E., aged 47, was admitted to the in-patient unit of thehospital because of the exacerbation of lumbosacral radiculitis. Withinthe framework of combined therapy he received, along with conventionalanti-inflammatory therapy, a 25% intranasal alcohol solution (a C30dilution) of monoclonal antiserum to FINLEPSIN (TEGRETOL)(5H-dibenz[b,f]azepin-5-carboxamide) in the form of 10 drops per dose.The next day the pain subsided and the excessive tension of back musclesreduced.

C. Patient T., aged 64, complained of insomnia and night cramps in hisextremities. Within the framework of combined therapy he was receivingorally at bedtime 20 ml of a C30 dilution of potentiated antiserum toPHENOBARBITAL (5-ethyl-5-phenyl-2,4,6(1H,3H,5H)-pyrimidinetrione). Athis new visit to the physician 10 days later the normalization of sleepwas noted along with a reliable reduction in the frequency of convulsivereactions.

D. Patient I., aged 45, with an established diagnosis of generalizedform of epilepsy had to give up taking LAMOTRIGINE(6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine) because of nausea.The prescription of a C30 homeopathic solution of monoclonal antibodiesto LAMOTRIGINE in the form of 10 intranasal drops 3 times a day insteadof LAMOTRIGIN made it possible to eliminate nausea and proceed with thecourse of treatment. There have been no generalized epileptic fits inthe course of 3-months' observation.

E. Patient U., aged 39, with an established diagnosis of epilepsy withrare absences was on PHENYTOINE (5,5-diphenyl-2,4-imidazolidinedione)treatment. She complained of dizziness and tremor for which reason andthe use of the preparation was discontinued. Instead the oral intake of20 ml of a D6 dilution of a potentiated antiserum to phenyloine 3 timesa day was prescribed. Two days later the patient felt better and hertremor disappeared. No absences were registered within 8 weeks ofobservation.

F. Patient P., aged 49, complained of pain and tension in hergastrocnemius muscles. She gave a history of sciatic neuralgia. In orderto reduce the patients muscular tension the physician prescribed an oralintake of 20 ml of a C30 homeopathized solution of monoclonal antibodiesto BACLOPHEN (β-(aminomethyl)-4-chlorobenzenepropanoic acid) 3 times aday in combination with anti-inflammatory therapy. At the new visit 7days later she stated that her muscular rigidity and pain subsided.

EXAMPLE 15 Potentiated Antibodies to Antiparkinsonian Drugs

A. Patient D., aged 76, with an established diagnosis of Parkinson'ssyndrome was taking a course of treatment with LEVODOPA(3-hydroxy-L-tyrosine). As the treatment was not very efficient, theadditional oral intake of a C15 dilution of monoclonal antibodies toLEVODOPA was prescribed in a dose of 1 tablet 3 times a day. Theelimination of tremor was registered 3 days later, which made itpossible to conclude that the therapy became more efficient. Threemonths later the patient was completely switched to therapy withantibodies. The tremor is insignificant. The general condition of thepatient is satisfactory.

B. Patient K., aged 69, with an established diagnosis of Parkinson'ssyndrome due to atherosclerosis of cerebral vessels complained of nauseaafter the intake of SELEGILINE (DEPRENYL)((R)—N,α-dimethyl-N-2-propenylbenzene ethanamine). The intranasaladministration of 10 drops of a D24 dilution of homeopathic solution ofantibodies to (R)—N,α-dimethyl-N-2-propenylbenzene ethanamine 3 times aday made it possible to eliminate nausea and to continue the course oftreatment with antibodies as monotherapy.

EXAMPLE 16 Potentiated Antibodies to Preparations Used Predominantly forthe Treatment of the State of Dependence

A. Patient B., aged 41, had been taking a course of treatment in orderto get rid of his habit of smoking. The intranasal administration of 20drops of a C1000 dilution of the antiserum to NICOTINE(S)-3-(1-Methyl-2-pyrrolidinyl)pyridine) 2 times a day was prescribed.The patient stated the lessening of his attraction to smoking after 4days of the treatment with the preparation.

B. Patient D., aged 19, was admitted to hospital on a suspicion of drugaddiction. Two hours after the oral administration of 3 ml of a C50homeopathic solution of antibodies to NALOXONE(5-α)-4,5-epoxy-3,14-dihydroxy-17-(2-propenyl)morphinan-6-onehydrochloride) the development of the withdrawal syndrome wasregistered, which was regarded as the naloxone-like effect. The furthertreatment with potentiated antibodies within the framework of combineddisintoxication therapy made it possible to arrest the state ofabstinence within 4 days.

C. Potentiated antibodies to DISULFIRAM (antabuse,(tetraethylthioperoxydicarbodiamide).

Patient E., aged 56, was admitted to the in-patient unit of a hospitalwith low blood pressure (80/50 mm Hg), suffering from nausea. Hepresented a history of alcohol intake against the background of ESPERAL(DISULFIRAM) treatment. Five hours after the intranasal administrationof 2 ml of a C30 solution of potentiated antibodies to DISULFIRAM thenormalization of the patients blood pressure and the control of nauseawere achieved; however, vegetative disorders reappeared when the alcoholtest was performed.

EXAMPLE 17 Potentiated Antibodies to Narcotic Analgesics

A. Patient Ch., aged 22, was admitted to the in-patient unit with signsof heroin withdrawal. In order to control his pain syndromeintramuscular injections of 1 ml of a C50 dilution of polyclonalantiserum to TRAMAL(trans-(++2-[(dimethylamino)methyl]-1-3(-metoxyphenyl)cyclohexanolhydrochloride) were given twice in the course of the first hour asmonotherapy. The arrest of the pain syndrome was virtually achieved.Conventional disintoxication therapy was prescribed.

B. Potentiated antibodies to BUTORPHANOL (MORADOL)(17-cyclobuthylmethyl)morphinan-3,14-diol).

Patient R., aged 24, was admitted to a narcological in-patient unit withan opiate withdrawal syndrome; the patient had been taking variousopiates for long time (6 months). The oral intake of 30 ml of a C200homeopathized solution of monoclonal antibodies to MORADOL 3 times a daylessened the intensity of the pain syndrome and the attraction to drugs.

C. Potentiated antibodies to PROMEDOL.

Patient S., aged 24, whose diagnosis was “heroin drug addiction,remission of a 7 months' duration” applied for medical advicecomplaining of pain in her right temporomandibular joint. No organiclesions were found after examination A D24 dilution of potentiatedantiserum to PROMEDOL, (1,2,5-trimethyl-4-phenyl-4-piperidinolpropanoate) was prescribed. After a single dose of the preparation thepain disappeared with background transitory manifestations of theso-called dry abstinence. When questioned, the patient reported theeasing of her attraction to heroin that had increased 10 days earlier.

D. Potentiated antibodies to MORPHINE(5α,6α)-7,8-didehydro-4,5-epoxy-17-methylmorphinan-3,6-diol.

Patient Z., aged 29, underwent appendectomy. In order to control thepostoperative pain he received a single 30 ml oral dose of a C30solution of potentiated antiserum to MORPHINE at bedtime. The patientwent to sleep. When questioned, he reported no feeling of euphoria uponthe intake of the preparation.

E. Potentiated antibodies to PHENTANYL(N-Phenyl-N-[1-(2-phenylethyl)-4-piperidinyl]propanamide).

Patient T., aged 68, complained upon admittance of pain in her spine.She had a history of metastases of stomach cancer into the vertebralbodies and of a long-time intake of narcotic analgesics. A slowintravenous infusion of 2 ml of a D12 solution of potentiated antibodiesto PHENTANYL twice a day was prescribed. After 4 days of the treatmentthe patient reported that the pain syndrome subsided.

EXAMPLE 18 Potentiated Antibodies to Anticholinesterase Drugs

A. Potentiated antibodies to PHYSOSTIGMINE((3aS-cis)-1,2,3a,8,8a-hexahydro-1,3a,8-trimethylpyrrolo[2,3-b]indole-5-olmethylcarbamate).

Patient F., aged 63, was under medical observation after a stroke.Objective findings: the muscular tension in the left arm was lowered.The intranasal administration of 0.5 ml of a C50 solution of potentiatedmonoclonal antibodies to PHYSOSTIGMINE 3 times a day was prescribedwithin the framework of combined therapy. After 3 weeks of the treatmentnormalization of the muscular tension and reflexes was observed.

B. Potentiated antibodies to PROSERINE(3-[[dimethylamino)carbonyl]-oxy]-N,N,N-trimethylbenzolaminium bromide).

Patient Ch., aged 60, after appendectomy suffered from the onset ofintestinal paresis in the postoperative period. The oral intake of aC200 dilution of the antiserum to PROSERINE in a dose of 1 tablet 3times a day was prescribed. After 4 days of the treatment the patient'sgastrointestinal tract motility was back to normal.

EXAMPLE 19 Potentiated Antibodies to Anti-Glaucoma Drugs

Patient Ya., aged 70, had had a long-time history of glaucoma. Thepatient had been taking ACETAZOLAMIDE (5-day courses of 250 mg every 6hours) to good effect. The preparation's mechanism of action involvescarbonic anhydrase blocking; on a prolonged use its efficacy is reduceddue to compensatory mechanisms. Therefore, it was found necessary todiscontinue the use of the preparation from time to time. During theseinterruptions of the treatment the attacks of glaucoma became morefrequent but the patient did not tolerate any other anti-glaucoma drugs.The prescription of a C6 dilution of potentiated antibodies toACETAZOLAMIDE in a dose of 1 tablet a day resulted in the restoration ofthe patients sensitivity to the preparation; his intraocular pressuredid not go beyond the upper bound of normal; the frequency of attacks ofglaucoma was markedly reduced. ACETAZOLAMIDE intake was discontinued.The term of follow-up was 4 months.

EXAMPLE 20 Potentiated Antibodies to Drugs Used for Migraine

A. Antibodies to DIHYDROERGOTAMINE.

Patient N., aged 41, complained of cramping pain in the left part of herhead. The diagnosis of migraine was established; the intranasaladministration of a. C200 dilution of potentiated monoclonal antibodiesto DIHYDROERGOTAMINE (5α,10α)-9,10-dihydro-12-hydroxy-2-methyl-5-(phenylmethyl)ergotamine-3,6,18-trione mesilate) 4 times a day was prescribed.At her next visit to the physician 7 days later the patient reported thelessening of both frequency and intensity of pain. It was recommended tocontinue the course of treatment.

B. Antibodies to SUMATRIPTANE(3-[2-(dimethylamino)ethyl-]-N-methylindole-5-methanesulfonamide).

Patient K., aged 42, addressed herself to an out-patient cliniccomplaining of attacks of headache localized in the left part of herhead and accompanied with nausea.

The prescription was to take orally 1 ml of a D24 solution ofpotentiated monoclonal antibodies to SUMATRIPTANE at the time of theattack of headache together with conventional analgesics. At her nextvisit to the physician the patient reported the disappearance of nauseaand the lessening of the intensity of pain.

EXAMPLE 21 Potentiated Antibodies to Local Anesthetics

A. Antibodies to LIDOCAINE((2-diethylamino)-N-(2,6-dimethylphenyl)acetamide).

Patient R. aged 32, complained of heart palpitation. The diagnosis ofventricular tachyarrhythmia was established on examination. Therecommendation was to take orally 1 tablet of a C12 dilution ofpotentiated antibodies to LIDOCAINE every hour during the attack. Usingthis drug, the patient reported normalization of the heart rhythm.

EXAMPLE 22 Potentiated Antibodies to Non-Steroid Antiinflammatory Drugs

A. Potentiated antibodies to DICLOFENAC(2-[(2,6-dichlorophenyl)amino]benzeneacetic acid).

Patient M., aged 52, complained of pain in his knees. The diagnosis ofarthritis in the phase of exacerbation was established on examination.The prescription was: compresses with a C6 homeopathic solution ofantibodies to DICLOFENAC. After four procedures the lessening ofhyperemia and soreness of the joints was noticed.

B. Potentiated antibodies to INDOMETHACINE.

Patient D., aged 48, complained of pain in the epigastric area. Hepresented a long-time (1.5 month) history of the intake of INDOMETHACINE(1-(4-chlorobenzoyl)-5-methoxy-2-methyl-1H-indole-3-acetic acid).Gastroscopy revealed erosive gastritis. The homeopathized solution of anantiserum to indomethacine (a C30 potency) in the form of 1 tablet 3times a day was prescribed. At a new examination 7 days later thepatient noted that the pain had disappeared.

C. POTENTIATED ANTIBODIES to CYCLOOXYGENASE.

Patient F., aged 49, had been suffering from rheumatoid polyarthritisfor 12 years. The use of NSAIDs of all groups including MOVALIS (apreparation with a relatively selective effect upon cyclooxygenase-2)was extremely problematic due to concomitant hyperacidic gastritis. Withthe background treatment with a D12 dilution of a potentiated form ofantibodies to cyclooxygenase-1 in a oral dose of 1 tablet 2 times a daythe patient tolerated MOVALIS well. The pain in his joints subsided andthe joint motility regained. The endoscopic examination showed theremission of hyperacidic gastritis.

D. POTENTIATED ANTIBODIES TO IBUPROFEN(α-methyl-4-(2-methylpropyl)benzeneacetic acid).

Patient L., aged 56, complained of pain and limited motility of herankle joint. The oral intake of IBUPROFEN in combination with theintranasal administration of 0.5 ml of a C12 dilution of potentiatedantibodies to α-methyl-4-(2-methylpropyl)benzolacetic acid twice a daywas prescribed. Five days later the normalization of joint motility andthe absence of pain were noted. Ibuprofen was discontinued. The patientstarted receiving potentiated antibodies as monotherapy. No inflammatorysymptoms or pain in her joints were found.

POTENTIATED ANTIBODIES TO ASPIRIN (2-(acetyloxy)benzoic acid).

E. Patient T., aged 48, complained of headaches. The examinationrevealed a temperature rise to 37.1° C. A C30 preparation of potentiatedantibodies to ASPIRIN in a dose of 1 tablet 4 times a day wasrecommended. Twenty-four hours later her body temperature was back tonormal and the headache subsided completely.

F. Patient T., aged 48, with an established diagnosis of ischemic heartdisease developed instable angina attacks at minimal physical strain.ACETYLSALICYLIC ACID (325 mg once a day) was among the preparations thepatient regularly took within the framework of combined therapy. Thepatient complained of stomach discomfort; a laboratory examinationrevealed the growth of the blood coagulation time from 5 to 12 minutes.The prescription was: 1 ml of a C12 dilution of potentiated antibodiesto ASPIRIN in the form of intramuscular injections once a day. Thestomach discomfort disappeared and the blood coagulation time shortenedto 8 minutes.

G. POTENTIATED ANTIBODIES to PARACETAMOL (N-(4-hydroxyphenyl)acetamide.

Patient N., aged 11, was admitted to the hospital with an acuterespiratory tract infection. The examination revealed a temperature riseto 38.2° C. and rhinitis. In addition to halazolin, the patient startedreceiving orally 10 ml of an aqueous solution of potentiated antibodiesto PARACETAMOL 4 times a day. Twelve hours later his body temperaturewas back to normal and rhinitis subsided.

EXAMPLE 23 Potentiated Antibodies to Pharmaceutical Agents Influencingthe Function of Respiratory Organs

A. Potentiated Antibodies to PHENOTEROL(1-(3,5-dioxyphenyl)-2-(para-oxy-α-methyl-phenetylamino)-ethanol).

Patient K., aged 22, suffering from asthmatic bronchitis used PHENOTEROL(berotec) in an aerosol form as his main therapeutic agent. The patientstated the reliability and efficiency of the preparation but complainedof hand tremor and heart palpitations associated with the medication.The use of a C30 dilution of potentiated antibodies to phenoterol in adose of 1 tablet 2 times a day improved the patient's tolerance for thepreparation without affecting its efficacy. Gradually the patient wasswitched to the potentiated preparation as monotherapy. No asthmaticepisodes were registered within 5 weeks of observation.

POTENTIATED ANTIBODIES to ATROVENT.

B. Patient A., aged 26, suffered from polyvalent allergy includingintolerance to soybeans and peanuts. He had been successfully receivingATROVENT (in the form of an inhalation solution) for frequent attacks ofbronchial asthma. After a single attempt to use ATROVENT in the form ofan inhalation aerosol the patient developed a severe anaphylacticreaction. The latter was arrested by means of three intranasaladministrations of 0.5 ml of a D24 dilution of antibodies to atroventwith 20-minutes intervals. Later on the patient started receiving 1tablet a day of a D12 dilution of antibodies to atrovent every morningas monotherapy. He was feeling well and had no attacks of bronchialasthma in the course of three months.

C. Patient A., aged 45, had been taking THEOPHYLLINE for a long time forthe attacks of bronchial asthma until he noted the loss of efficiency ofthe preparation. The oral intake of a C30 dilution of a potentiatedsolution of antibodies to THEOPHYLLINE (1,3-dimethylxanthine) in a doseof 1 tablet 2 times a day enhanced the efficacy of the therapy, whichallowed the dose of theophylline to be reduced.

D. Patient D., aged 36, had been suffering from bronchial asthma sincethe age of 19. As his attacks occurred at night, he split his daily doseof 600 mg of THEOPECK into ⅔ in the evening and ⅓ in the morning. Thepatient complained of excessive irritability and the worsening of sleep.An attempt to reduce the dose of the preparation did not result inbetter sleep but nocturnal asthmatic fits became more frequent. Once thetreatment with a C30 dilution of homeopathized antibodies totheophylline in a dose of 1 tablet 2 times a day had been started, thepatients sleep returned to normal within 3 weeks. The dose oftheophylline was reduced to 300 mg, the asthmatic fits became rare.

E. POTENTIATED ANTIBODIES to MENTHOL (2-isopropyl5-methylcyclohexanol-1).

Patient Ch., aged 39, complained of cough and dryness in his throat. Therecommendation was to take a tablet of potentiated antibodies to MENTHOL(a C12 dilution) at the onset of a coughing fit. At the next visit thepatient reported the efficiency of the preparation for controlling thecough. It was recommended to continue the course of treatment.

Potentiated antibodies to adrenomimetic drugs

F. Potentiated antibodies to NAPHTHIZINE, (NAPHAZOLINE)(4,5-dihydro-2-(1-naphthalinemethyl)-1H-imidazole).

Patient V., aged 49, complained of tachycardia after administration ofnaphthizine for rhinitis. Naphtizine was replaced by a homeopathicsolution (a C6 dilution) of monoclonal antibodies to4,5-dihydro-2-(1-naphthalinemethyl)-1H-imidazole in a dose of 1 tablet 3times a day. The patient reported normalization of his cardiac rhythm,which made it possible to continue taking the preparation. Twenty-fourhours after the beginning of the treatment rhinorrhea virtuallydisappeared.

G. Potentiated antibodies to SALBUTAMOL(α1-[[(1,1-dimethylethyl)amino]methyl]-4-hydroxy-1,3-benzenedimethanol).

Patient I., aged 54, complained of hard breathing fits. The intranasalinstillations of a C50 homeopathic solution of antibodies to SALBUTAMOLin the form of 5 drops of an aqueous solution 3 times a day wereprescribed. The use of the preparation made it possible to shorten theduration of hard breathing fits.

EXAMPLE 24 Potentiated Antibodies to Histamine and Antihistamine Drugs

A. Potentiated antibodies to CROMOLYN(5,5-[(2-hydroxy-1,3-propanediyl)-bis-(oxy)]-biz-[4-oxo-4H-1-benzopyrane-2-carboxylicacid).

Patient M., aged 57, had been suffering from seasonal pollinosis. Theprescription of 1 ml of a C30 dilution of potentiated antibodies toCROMOLYN in the form of nasal drops 2 times a day made it possible tocontrol the symptoms of rhinitis.

B. Potentiated antibodies to ZADITEN (KETOTIFEN)(4,9-dihydro-4-(1-methyl-4-piperidinylidene-10H-benzo[4,5]cyclohepta[1,2-b]-thiophen-10-onehydrofumarate).

Patient M., aged 29, a software programmer by profession has beensuffering from pollinosis with symptoms of kerato-conjunctivitis duringspring and summer. He used to control exacerbations of his conditionwith 1 mg of ZADITEN (1 tablet) 2 times a day. The positive therapeuticeffect of ZADITEN intake was accompanied by a depressed intensity ofemotional and physical reactions, somnolence and listlessness. Theadministration of a C30 dilution of potentiated antibodies to ZADITEN ina dose of 1 tablet 2 times a day resulted in the elimination ofZADITEN's side effects. The ZADITEN intake was discontinued; the patientcontinued to receive the potentiated preparation as monotherapy. Nomanifestations of hay fever were noted afterwards.

C. Potentiated antibodies to TAVEGYL(1-methyl-2[2-(α-methyl-para-chlorbenzhydryl-oxy)-ethyl]-pyrrolidine).

Patient Ch., aged 35, used to take TAVEGYL to good effect for chronicurticaria. The parenteral administration of TAVEGYL (in a dose of 2 mlintramuscularly) in the case of the next exacerbation accompanied by apronounced allergic skin syndrome and a high eosinophile count (18%) inthe peripheral blood resulted in a rapid clinical and laboratoryimprovement (eosinophile count going down to 7%); however, headache,nausea, and mouth dryness were noted. The administration of a C12dilution of potentiated polyclonal antibodies to TAVEGYL in a dose of 1tablet 2 times a day resulted in the elimination of the side effects ofTAVEGIL use. Further on, the patient has been receiving TAVEGIL incombination with potentiated antibodies to TAVEGIL; a month later shewas put on a maintaining dose of antibodies (once in three days) asmonotherapy.

D. Patient S., aged 48, was admitted to the pulmonology unit forpneumonia. The patient had an anaphylactic shock in response to theintravenous injection of calcium chloride. The intramuscular injectionof 1 ml of C50 dilution of potentiated antibodies to HISTAMINE made itpossible to arrest the symptoms of shock within 5 minutes.

E. POTENTIATED ANTIBODIES to KETOTIFEN(4,9-dihydro-4-(1-methyl-4-piperidinylidene)-10H-benzo[4,5]cyclohepta[1,2-b]thiophen-10-onehydrofumarate).

Patient D., aged 12, was hospitalized because of his complaint of heavybreathing during the season of poplar blossoming. The oral intake of 10ml of a C24 dilution of homeopathic solution of antiserum to KETOTIFEN 3times a day restored the patient's respiratory function to the normallevel.

Potentiated antibodies to inhibitors of H1-histamine receptors.

F. Potentiated antibodies to LORATIDINE (CLARITINE) (ethyl ester of4-(8-chloro-5,6-dihydro-11H-benzo-[5,6]cyclohepta[1,2-b]pyridin-1-ylidene-)-1-piperidinecarboxylic acid).

Patient K., aged 45, complained of an itching sensation in hernasopharynx after working with paintwork materials. After theadministration of a C200 dilution of potentiated monoclonal antibodiesto LORATIDINE (in a dose of 1 tablet 2 times a day) itching subsided. Itwas concluded that the preparation had proved its efficiency.

Potentiated antibodies to TAVEGYL (CLEMASTINE)([R—(R*,R*)]-2-[2-[1-(4-chlorophenyl)-1-phenylethoxy]ethyl]-1-methylpyrrolidinefumarate or1-methyl-2[2-α-methyl-para-chlorbenzhydryl-oxy)-ethyl]-pyrrolidinefumarate).

Patient P., aged 34, complained of somnolence after the intake ofTAVEGIL for the itching of her elbows. The oral intake of a D6 dilutionof potentiated antibodies to[R—(R*,R*)]-2-[2-[1-(4-chlorophenyl)-1-phenyl-ethoxy]ethyl]-1-methylpyrrolidinefumarate in a dose of 1 tablet 2 times a day was recommended. At hernext visit to the physician the patient reported that her drowsiness hadsubsided and her mood improved. She was put on the potentiatedpreparation as monotherapy. At her visit to the physician 2 months laterthe patient reported that her itching had virtually disappeared.

EXAMPLE 25 Potentiated Antibodies to Medications Used for Treatment ofErosive Lesions of Gastrointestinal Tract

Potentiated ANTIBODIES to inhibitors of H2-histamine receptors.

A. Potentiated Antibodies to RANITIDINE(N-[2]-[[[5-[(Dimethylamino)methyl]-2-furanyl]methyl]thio]ethyl]-N-methyl-2-nitro-1,1-ethendiamine).

Patient N., aged 56, complained of epigastric pain. The prescriptionwas: 1 tablet of a C12 dilution of a potentiated polyclonal antiserum toRANITIDINE(N-[2]-[[[5-(dimethylamino)methyl]-2-furanyl]-methyl]-thio]-ethyl]-N-methyl-2-nitro-1,1-ethendiamine)to be taken after meals. After 3 days of the treatment the paindisappeared.

B. Potentiated antibodies to FAMOTIDINE(3-[[[2-[(aminoiminomethyl)-amino]-4-thiazolyl]-methyl]-thio]-N-(aminosulfonyl)-propaneimidamide).

Patient G., aged 45, complained of nausea after meals. Gastroscopyrevealed gastritis in an exacerbation phase. The recommendationsinvolved diet and the oral intake of 10 ml of a C30 solution ofpotentiated polyclonal antibodies to FAMOTIDINE before meals. After 5days of the treatment the patients general condition and thegastroscopic pattern of his gastric mucosa were back to normal.

Potentiated antibodies to proton pump inhibitors

C. Potentiated antibodies to OMEPRAZOLE(5-metoxy-2-[[(4-metoxy-3,5-dimethyl-2-pyridinyl)methylsulfonyl]1H-benzimidazole).

Patient U., aged 33, felt a pronounced pain in the pit of the stomachfrom time to time. Gastroscopy revealed erosive gastritis. After theadministration of a C12 homeopathic dilution of the preparation ofpolyclonal antibodies to OMEPRAZOLE in a dose of 1 tablet-3 times a dayalong with a diet the gastric mucosa was back to normal 6 days: laterand both frequency and intensity of pain diminished.

D. Patient A., aged 44, with an established diagnosis of ulcerativedisease of stomach and duodenum in the phase of exacerbation had beentaking OMEZ (20 mg daily, a proton pump inhibitor) for 4 weeks. Againstthe background of an improvement of the course of the disease thepatient complained of dizziness and headache. The treatment with a D12dilution of potentiated antibodies to OMEZ in a dose of 1 tablet 3 timesa day resulted in the elimination of side effects on the part of thecentral nervous system and in the improvement of the patients generalcondition within 3 days. Later on, the remission was maintained solelyby the intake of potentiated antibodies to OMEZ.

Potentiated antibodies to M-cholinolytic drugs.

E. Potentiated antibodies to PIRENZEPINE (GASRTOZEPINE)(5,11-dihydro-11-[(4-methyl-1-piperazinyl)acetyl]-6H-pyrido[2,3-b][1,4]benzodiazepine-6-one).

Patient P., aged 57, complained of tremor and pain in the pit of hisstomach after meals. Gastroscopy revealed no organic lesions of stomachmucosa. The oral intake of a D8 homeopathic solution of antiserum toGASRTOZEPINE in a dose of 1 tablet before meals was recommended. A newexamination 10 days later showed an improvement of the patients mood; noepigastric pain was noted. It was concluded that the preparation wasefficient.

F. Potentiated antibodies to ATROPINE(8-methyl-8-azabicyclo[3.2.1.]oct-3-yl ester ofendo-(+−)-α-(hydroxymethyl)benzolacetic acid).

Patient M., aged 41, suffered of cramps in his right subcostal area 2hours after meals rich in fat. The prescription was: a diet and the oralintake of a C200 aqueous solution of potentiated polyclonal antibodiesto ATROPINE in a dose of 10 ml (after meals). The pain syndrome subsided2 days later. It was recommended to continue the course of treatment.

G. Patient F., aged 42, suffered from sinus bradycardia; his pulse ratewas 48 beats/min. He had been taking the BELLADONNA EXTRACT in tablets;the positive therapeutic effect of the extract (the pulse rate increasedto 64 beats/min) was accompanied by general weakness and dryness of skinand mucosae. (ATROPINE, the active principle of the extract, is thetropinic ester of d,l-tropic acid; the L isomer is active whereas the Disomer manifests low activity). The recommendation was to takealternately potentiated antibodies (a C15 dilution) to both isomers. Thepatient's pulse rate stabilized at 64 beats/min; no cholinolytic sideeffects were observed.

H. Antibodies to NO-SPA (drotaverine)([(3,4-diethoxyphenyl)methylene]-6,7-diethoxy-1,2,3,4-tetrahydroisoquinoline).

Patient L., aged 38, complained of epigastric pain and belching. Hisexamination revealed no organic lesions. The prescription was: the oralintake (before meals) of an aqueous solution (a C6 dilution) ofmonoclonal antibodies to NO-SPA (drotaverine) in a dose of 15 ml. After2 days of the treatment the patient stated the lessening of dyspepticmanifestations.

EXAMPLE 26 Potentiated Antibodies to Antiemetic Drugs

A. Potentiated antibodies to DOMPERIDONE (MOTILIUM)(5-Chloro-1-[1-[3-(2,3-dihydro-2-oxo-1H-benzimidazol-1-yl)propyl]-4-piperidinyl]-1,3-dihydro-2H-benzimidazol-2-one).

Patient N., aged 71, had been treated with levodopa for parkinsonism andhad to stop the therapy because of nausea and vomiting. The oral intakeof levodopa in combination with 30 ml of a C30 dilution of an aqueoussolution of potentiated monoclonal antibodies to MOTILIUM wasprescribed, which made it possible to eliminate vomiting and continueantiparkinsonic therapy.

B. Patient Zh., aged 64, developed nausea and vomiting in response toradio- and chemotherapy he had been getting for peripheral lung cancer.The prescription of MOTILIUM controlled symptoms of dyspepsia but thepatient developed weakness, drowsiness, and intestinal cramps. MOTILIUMwas discontinued and a C6 dilution of potentiated antibodies to MOTILIUMwas administered in a dose of 1 ml intramuscularly 2 times a day, whichresulted in the elimination of neurotoxic and spastic reactions. Thetreatment was continued with a positive clinical effect.

C. Patient Yu., aged 55, suffered from chronic gastritis andesophagitis. He had been taking MOTILIUM (the active principle isDOMPERIDONE, an antagonist of dopamine receptors) for 3 months in a doseof 10 mg 15-20 minutes before meals on his own initiative under theinfluence of commercial advertising. He sought for medical advicebecause of gynecomastia he had noticed. Motilium was discontinued and aC1000 dilution of potentiated antiidiopathic antibodies to DOMPERIDONEwas prescribed for 2 months in a dose of 1 tablet a day. The symptoms ofgynecomastia disappeared and dyspeptic problems never resumed.

D. Potentiated antibodies to METOCLOPRAMIDE (REGLAN, CERUCAL)(4-amino-5-chloro-N-[2-(diethylamino)ethyl]-2-metoxybenzamide).

Patient D., aged 38, complained of nausea and belching after meals. Acourse of treatment with an oral preparation containing a C30 dilutionof potentiated antibodies to METOCLOPRAMIDE (REGLAN, CERUCAL) in a doseof 2 tablets before meals was prescribed. Four days later the patientreported the disappearance of nausea. A conclusion about the efficiencyof the preparation was drawn.

EXAMPLE 27 Potentiated Antibodies to Antitussive Drugs

A. Potentiated antibodies to CODEINE((5α,6α)-7,8-didehydro-4,5-epoxy-3-methoxy-17-methylmorphinan-6-ol).

Patient B., aged 47, complained of fits of dry cough. The diagnosis was:chronic bronchitis; the intranasal administration of a C200 dilution ofan aqueous solution of potentiated monoclonal antibodies to CODEINE in adose of 5 drops during a fit was recommended. Twenty-four hours afterthe beginning of the treatment the elimination of cough was registered.

B. Potentiated antibodies to LIBEXIN (PRENOXDIAZINE)(1-[2-[3-(2,2-diphenylethyl)-1,2,4-oxydiazol-5-yl]ethyl]piperidine).

Patient T., aged 41, had been taking LIBEXIN tablets for her cough. Shecomplained of dryness in her mouth and throat. LIBEXIN was discontinued.The suggestion was to take orally a C50 dilution of a potentiatedantiserum to1-[2-[3-(2,2-diphenylethyl)-1,2,4-oxydiazol-5-yl]ethyl]piperidine in adose of 1 tablet 3 times a day. The administration of the homeopathicpreparation eliminated the undesired symptoms within 2 hours. Theexamination two days later showed a satisfactory general condition ofthe patient and the absence of cough.

EXAMPLE 28 Potentiated Antibodies to Various Groups of AntihypertensiveDrugs

Potentiated antibodies to sympatholythics.

A. Potentiated antibodies to RESERPINE

Patient B., aged 36, had been taking a course of treatment with ADELPHANfor arterial hypertension. After 3 weeks of the treatment she startedcomplaining of dizziness. The examination revealed that her bloodpressure had dropped to 105/60 mm Hg. ADELPHAN was discontinued. Theoral intake of a C12 dilution of potentiated antiserum to RESERPINE in adose of 1 tablet 2 times a day was prescribed. Two days later herdizziness subsided and the blood pressure rose to 115/70 mm Hg.

B. Patient P., aged 72, suffered from hypertensive disease, Stage II b.She had been taking RAUNATINE (1 tablet 2 times a day) for a long timeto good effect. The patient complained of dizziness and stuffiness inher nose not associated with a common cold. A C50 dilution ofpotentiated antibodies to RESERPINE was prescribed; this agent lessenedher dizziness and completely eliminated stuffiness in her nose. Lateron, she had been taking the preparation for 3 months in a dose of 1tablet 2 times a day. Her blood pressure stabilized at a level of 140/90mm Hg.

Potentiated antibodies to α-adrenolytic drugs.

C. Potentiated antibodies to PRAZOSIN (MINIPRESS)(1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-(2-furanylcarbonyl)piperazine).

Patient Ch., aged 53, complained of headaches after the intake ofPRAZOSIN for hypertensive disease. The prescription of a C30 dilution ofa potentiated antiserum to(1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-(2-furanylcarbonyl)piperazine)in a dose of 1 tablet together with the intake of the PRAZOSIN resultedin the lowering of the patients blood pressure. Later on, he started theadministration of the antibodies as monotherapy; the blood pressure didnot rise above his optimal level of 150/90 mm Hg.

D. Patient I., aged 64, with an established diagnosis of arterialatherosclerosis (predominantly of the vessels of his lower extremities)and hypertensive disease, Stage IIb, had been taking PRAZOSIN in a doseof 8 mg a day (16 tablets). The patient complained of nausea andconstant drowsiness. An attempt to reduce the dose on his own initiativeresulted in a rise of the blood pressure and reappearance of the pain inhis legs. The administration of a C12 dilution of potentiated antibodiesto PRAZOSIN in a dose of 1 tablet 3 times a day made it possible toeliminate the undesirable manifestations and to reduce the dose ofPRAZOSIN to 10 mg a day. Two months later the patient switched to themaintaining dose of 1 tablet a day of a C50 dilution of potentiatedantibodies to PRAZOSIN.

E. Patient Shch., aged 69, has been receiving 1 tablet of OMNIC (400 mgafter breakfast) for benign hyperplasia of the prostate. The patientdeveloped symptoms of orthostatic hypotension. The treatment with a C30dilution of potentiated antibodies to OMNIC in a dose of 1 tablet 3times a day was begun. Orthostatic symptoms disappeared 2 days laterwhereas the therapeutic effect of the preparation was preserved: thepatient felt better, the volume of the residual urine diminished and thefrequency of urinations reduced.

Potentiated antibodies to CLOFELINE(2,6-dichloro-N-2-imidazolidinylidenbenzamine)

F. Patient E., aged 58, complained of drowsiness after theadministration of CLOFELINE she had been taking for hypertensivedisease. The recommendation was to combine the intake of CLOFELINE and aC12 solution of monoclonal antibodies to2,6-dichloro-N2-imidazolidinylidenbenzamine in a dose of 1 tablet 3times a day. After two days of the treatment the patient stated theimprovement of her mood and an enhanced motor activity. CLOFELINE wasgradually discontinued. Now the patient receives only the potentiateddrug; the arterial blood is stable.

G. Patient Yu., aged 59, had a 10-years' history of essentialhypertension. A regular intake of CLOFELINE in a dose of 0.6 mg a dayproduced a favorable effect on the course of his illness. He sought formedical advice at his district out-patient clinic because of dryness inthe mouth. Several weeks of the administration of a C200 dilution ofpotentiated antibodies to CLOFELINE in a dose of 15 drops of an aqueoussolution 4 times a day resulted in the elimination of the undesirablemanifestations. The patient was switched to the potentiated preparationalone as the maintaining therapy.

Potentiated antibodies to isomers of NEBILET.

H. Patient R., aged 63, with an established diagnosis of hypertensivedisease, Stage IIa, was on NEBILET treatment (the drug contains twoisomers; both are biologically active but their metabolization ratevaries in different people). The patient complained of nightmares, whichhad not been experienced before the NEBILET administration.Pharmacokinetic studies showed that the patient belonged to the groupwith a slow type of metabolism (high difference in the concentrations ofL- and D-enantiomers in the plasma). The administration of a D24dilution of potentiated antibodies to L-isomer in a dose of 1 tablet 3times a day resulted in the normalization of sleep along with theconservation of a good hypotensive effect.

I. Patient P., aged 67, has been taking LABETALOL (400 mg a day) forhypertensive disease. The patient complained of heavy breathing. A C15dilution of potentiated antibodies to RR-isomer in an oral dose of 10 mltwo times a day was prescribed. After two days of treatment thepatient's condition improved and functional tests showed the improvementof bronchial conduction.

Potentiated antibodies to inactive isomers of LABETALOL.

J. Patient A., aged 57, with an established diagnosis of hypertensivedisease and ischemic heart disease took LABETALOL and complains of heavybreathing and dizziness. The prescription was: a mixture of a C30dilution of potentiated antibodies to inactive isomers in a dose of 1sachet of powder a day. The patients condition improved and the dose ofthe drug was reduced from 400 mg to 50 mg a day.

K. Patient Ya., aged 61, with an established diagnosis of hypertensivedisease and ischemic heart disease took APRESSIN (HYDRALAZINE)(1-hydrazinophthalazine hydrochloride) 250 mg a day in 4 doses. Shecomplained of headaches, hot flashes, and nausea. An attempt to reducethe dose did not result in the desired effect. The recommendation wasstart taking a D8 dilution of potentiated monoclonal antibodies to thehydrazine group of the APRESSIN molecule; this group is capable ofinhibiting the inactivation of endogenous vasodilating factors (NO inparticular). After two days of treatment with this preparation in a doseof 1 tablet before meals the patient noticed the improvement of hercondition. The treatment with APRESSIN was continued; its dose wasreduced without any attenuation of its pronounced therapeutic effect andtwo months later APRESSIN was discontinued. The patient was put onmonotherapy with the antibodies.

Potentiated antibodies to calcium channel blockers.

Potentiated antibodies to NORVASK (AMPLODIPINE) (3-ethyl-5-methyl esterof2-[(2-aminoethoxy)methyl]-4-(2-chlorophenyl)-1,4-dihydro-6-methy-l-3,5-pyridinedicarboxylic acid).

B. Patient Ch., aged 59, took NORVASK for hypertensive disease. Hecomplained of headache after the intake of the preparation. Theprescription was: the intranasal administration of 1 ml of a C1000dilution of potentiated antiserum to 3-ethyl-5-methyl ester of2-[(2-aminoethoxy)methyl]-4-(2-chlorophenyl)-1,4-dihydro-6-methyl-3,5-pyridinedicarboxylic acid once a day in the form of 10 drops to be taken 3 timesa day. The next day his headache disappeared. The patient kept takingthe two medications together. Six months later the patient was put onmonotherapy with the potentiated preparation.

Potentiated antibodies to the antagonists of ACE and of angiotensin-2receptors.

Potentiated antibodies to CAPTOPRIL((S)-1-(3-mercapto-2-methyl-1-oxopropyl)-L-proline):

M. Patient L., aged 40, complained of periodical headaches and episodesof hypertension. The oral intake of a C50 homeopathic solution ofpotentiated anti-bodies to CAPTOPRYL in a dose of 5 ml 2 times a day wasrecommended. Within 10 days of the treatment a decrease in the frequencyof headaches was noticed.

Potentiated antibodies to LOSARTAN (COZAAR)(2-butyl-4-chloro-1-[[2-(1H-tetrazol-5-yl)[1,1′-biphenyl]-4-yl]methyl]-1H-imidazole-5-methanol).

N. Patient G., aged 46, complained of tremor. He had a history ofLOSARTAN intake for his hypertensive disease. The recommendation was totake a D24 dilution of potentiated antibodies to2-butyl-4-chloro-1-[[2-(1H-tetrazol-5-yl)[1,1′-biphenyl]-4-yl]methyl]-1H-imidazole-5-methanolin a dose of 1 tablet 2 times a day. After three days of the treatmentthe tremor disappeared. Later on, in order to keep his blood pressurestable the patient received only potentiated antibodies.

O. Patient E., aged 42, with an established diagnosis of essentialarterial hypertension had been taking MOXONIDINE in a dose of 300 mg aday. The patient complains of dryness in his mouth and drowsiness. Thetreatment with a C30 dilution of potentiated antibodies to MOXONIDINEproduced a positive effect. Later on, the patient was put on preventivetreatment with antibodies to MOXONIDINE in a dose of 1 tablet a day.

P. Patient M., aged 58, with an established diagnosis of essentialarterial hypertension, Stage 11b had been taking ENALAPRIL(1-[N—[S]-1-carboxy-3-phenylpropyl]-L-alanyl]-L-proline-1′-ethyl ester),an angiotensin-converting enzyme inhibitor) on her physician's advice ina dose of 20 mg once a day. She complains of cough and dyspepsia. Thepatient used to take medications for the treatment of the intestinalmicroflora disorder on her own initiative with no positive results. Thebacteriological testing of her intestinal microflora yielded nopathological findings: ENALAPRIL was discontinued. The new therapyscheme included the addition of a C200 dilution of potentiatedantibodies to ENALAPRIL in a dose of 1 tablet once a day. The patientsbowel function normalized and the cough ceased.

Q. Patient Z., aged 47; with an established diagnosis of hypertensivedisease had been taking VALSARTAN in a dose of 80 mg a day. Shecomplained of incessant cough and pharyngitis. Neither X-ray examinationnor phthisiologists and otolaryngologists consultations revealed anypathology. The administration of C30 potentiated antibodies to VALSARTANin a dose of 1 tablet 2 times a day eliminated the side effects of thepreparation. After that the dose of VALSARTAN was reduced first to 40 mga day and later to 20 mg a day with a stable hypotensive effect.

Potentiated antibodies to DILTIAZEM.

R. Patient C., aged 54, with an established diagnosis of hypertensivedisease, ischemic heart disease, angina decubitus had been takingDILTIAZEM in a dose of 40 mg 4 times a day with good clinical effect.Rare attacks of angina: about once a week. After 1.5 month of treatmentthe patient noticed the slowing of the pulse rate (from 72 to 48-52beats/min); the ECG indicated the extension of the P-Q interval from0.12 to 0.20 s. The treatment with a D24 dilution of potentiatedpolyclonal antibodies to DILTIAZEM in a dose of 1 tablet 3 times a daywas prescribed. The patient's pulse rate reached 60 beats/min, the P-Qinterval shortened to 0.15 s, without angina attacks becoming morefrequent. The dosage of DILTIAZEM was reduced to 20 mg 2 times a day.

Potentiated antibodies to spasmolytic drugs.

Potentiated antibodies to DIBAZOLE (2-(phenylmethyl)-1H-benzimidazole).

S. Patient Z., aged 41, complained of headache and nausea. The diagnosisof hypertensive disease was established and the oral intake of a C12homeopathic solution of polyclonal antibodies to DIBAZOLE in a dose of 1tablet 2 times a day was recommended. Ten days later the patientreported feeling better and not suffering from headaches.

EXAMPLE 29 Potentiated Antibodies to Substances Taking Part in NaturalRegulation of the Blood Pressure

A. Patient S., aged 46, had been sent to hospital within several yearsbecause of hypertension crises. Once a crisis had been arrested thepatient was put on the maintaining therapy with captopril. In order toenhance the hypotensive effect a C12 dilution of potentiated antibodiesto RENIN in a dose of 1 tablet 2 times a day was added to the treatment.Combined therapy made it possible for the first time in many years tolower the patients blood pressure to 140/100 mm Hg. The patient'scondition is satisfactory.

B. Patient H., aged 38, suffered from therapy-resistant essentialhypertension. The closest to optimal drug for the patient was ENALAPRIL,which made it possible to stabilize the blood pressure at 160/110 mm Hg.The treatment protocol with an added intake of a D24 dilution ofpotentiated polyclonal antibodies to ANGIOTENSIN-CONVERTING ENZYME (in adose of 15 drops of alcohol solution 3 times a day) made it possible tolower the patients systolic pressure to 120-130 mm Hg. The patient hadnot presented any complaints for 2 months.

C. Patient D., aged 19, had been suffering from therapy-resistantarterial hypertension for 6 months. The use of a C12 dilution ofpotentiated antibodies to ANGIOTENSIN II in a dose of 1 tablet 2 times aday made it possible to stabilize the patient's condition: nocomplaints, the blood pressure reached 120/75 mm Hg.

EXAMPLE 30 Potentiated Antibodies to Diuretic Drugs

Potentiated antibodies to FUROSEMIDE(5-(aminosulfonyl)-4-chloro-2-[(2-furanylmethyl)]aminobenzoic acid).

A. Patient D., aged 67, had been taking a course of treatment withFUROSEMIDE for edemata caused by cardiac failure. She complained ofnausea and the lack of appetite. Furosemide was discontinued. Therecommendation was to start the oral intake of a C30 aqueous solution ofpotentiated monoclonal antibodies to5-(aminosulfonyl)-4-chloro-2-[(2-furanylmethyl)]aminobenzoic acid 2times a day in a dose of 20 ml. A new examination 7 days later revealedthe improved appetite, the absence of nausea and edemata.

Potentiated antibodies to HYPOTHIAZIDE(6-chloro-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide-1,1-dioxide).

B. Patient N., aged 64, with established diagnosis of hypertensivedisease had been taking HYPOTHIAZIDE. The patient noticed a decrease inthe efficacy of the preparation; hence, HYPOTHIAZIDE was discontinued.The recommendation was to start the oral intake of a C200 dilution of apotentiated antiserum to HYPOTHIAZIDE in a dose of 1 tablet 3 times aday, which made it possible to pre-serve the diuretic effect afterHYPOTHIAZIDE had been discontinued.

EXAMPLE 31 Potentiated Antibodies to Cardiotropic Drugs

Potentiated antibodies to nitrates.

Potentiated antibodies to NITROSORBIDE (1,4,3,6-dianghydrido-D-glucitoldinitrate).

A. Patient Sh., aged 52, suffering from hypertensive disease complainedof headache after the first intake of NITROSORBIDE. In addition to theconventional treatment, the oral intake of a C20 dilution of potentiatedantiserum to NITROSORBIDE was prescribed in a dose of 10 ml 3 times aday. Seven days later the patient reported an improved tolerance toNITROSORBIDE and the lessening of pain.

Potentiated antibodies to NITROGLYCEROL.

B. Patient U., aged 71, had been taking NITROSORBIDE (40 mg a day, 4tablets) for 5 weeks for ischemic heart disease and angina of effortalong with NITROGLYCEROL as needed (up to 8-10 tablets a day). Withinthe last week the dose of NITROSORBIDE was increased to 6 tablets, andthat of NITROGLYCEROL, to 15-16 tablets as the angina attacks grew morefrequent. The prescription was to take a C6 dilution of potentiatedantibodies to NITROGLYCEROL in a dose of 1 tablet 2 times a day. After 5days of treatment a marked reduction in the frequency of attacks wasachieved, which made it possible to reduce the dose of NITROSORBIDE to 4tablets and that of NITROGLYCEROL to 1-2 tablets a day.

Potentiated antibodies to Cytochromes a+a3.

C. Patient G., aged 39, was admitted to hospital with the diagnosis ofhypertensive disease, ischemic heart disease, cardiac failure due tomyocardial infarction; he had been treated with intravenous infusions ofSODIUM NITROPRUSSIDE (sodium nitrozylpentacyanoferrate) in a dose of 100mg a day for 4 days. By the 5^(th) day the hypotensive effect of thepreparation had significantly decreased as sodium cyanide accumulatingas a result of SODIUM NITROPRUSSIDE metabolism played an important partin the pharmacological effect of the preparation. (Cyanides act asblockers of the mitochondria respiratory chain at the level ofCytochrome a+a3). The administration of a C200 dilution of potentiatedpolyclonal antibodies to CYTOCHROMES a+a3 in a dose of 1 tablet 3 timesa day restored the efficacy of SODIUM NITROPRUSSIDE.

Potentiated antibodies to β-adrenoblockers.

Potentiated Antibodies to ATENOLOL(4-[2-hydroxy-3-[(1-methylethyl)amino]propoxy]benzeneacetamide).

D. Patient E., aged 32, complained of episodes of tachycardia caused byoverfatigue. Electrocardiography revealed no organic lesions. ATENOLOLwas discontinued. The oral intake of a C12 dilution of a potentiatedantiserum to ATENOLOL was prescribed. The intake of the preparation in adose of 1 tablet 2 times a day resulted in a decrease both in theintensity and duration of episodes of tachycardia 5 days after thebeginning of treatment.

Potentiated antibodies to ANAPRILIN (PROPRANOLOL)(1-[(1-methylethyl)amino]-3-(1-naphthalenyloxy)-2-propanol).

E. Patient I., aged 54, sought for medical advice for periodic heavybreathing. She presented a history of a regular intake of ANAPRILIN(PROPRANOLOL). The intranasal administration of a C12 dilution of apotentiated solution of monoclonal antibodies to1-[(1-methylethyl)amino]-3-(1-naphthalenyloxy)-2-propanol in a dose of0.5 ml 2 times a day was prescribed as monotherapy. A new examination 7days later showed an improvement of the respiratory function. Aconclusion about the efficacy of the homeopathic preparation was drawn.

F. Patient A., aged 57, developed bradyarrhythmia withMorgagni-Adams-Stokes attacks after myocardial infarction. To preventattacks she took ORCIPRENALINE (½ tablet 6 times a day) and complainedof nausea, dryness in her mouth, and the tremor of her hands. Thetreatment with a D3 dilution of potentiated monoclonal antibodies toORCIPRENALINE (in a dose of 1 tablet 3 times a day) made it possible toeliminate the unpleasant sensations; the attacks of arrhythmia stoppedrecurring.

Potentiated antibodies to cardiac glycosides.

Potentiated antibodies to DIGITOXIN((3β,β3)-3-[(O-2,6-dideoxy-β-D-ribo-hexapyranosyl-(1-4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl)-(1-4)-2,6-didesoxy-β-D-ribo-hexapyranosyl)oxy]-14-hydroxycard-20(22)-enolide).

G. Patient B., aged 68, had been taking a course of treatment withDIGITOXIN for cardiac failure complained of nausea associated with theintake of the preparation. The additional prescription was the oralintake of a C200 dilution of a potentiated preparation of polyclonalantibodies to((3β,5β)-3-[(O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1-4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl)-(1-4)-2,6-dideoxy-β-D-ribo-hexapyranosyl)oxy]-14-hydroxycard-20(22)-enolide)in a dose of 1 tablet 2 times a day. After two days of the treatment thepatient noticed the disappearance of nausea. The intake of thehomeopathic preparation made it possible to improve the patient'stolerance of DIGITOXIN and to reduce gradually its dose to ¼ of a tablet2 times a day.

H. Patient Ch., aged 31, with an established diagnosis of chroniccardiac failure caused by rheumatic heart disease had been taking themaintaining dose of DIGITOXIN 0.75 mg a day (3 tablets). She sufferedfrom permanent nausea and periodical vomiting. An attempt to reduce thedose of DIGITOXIN resulted in the enhancement of manifestations ofcardiac failure, edema in the first place. With DIGITOXIN discontinued,the patient started receiving a D6 dilution of potentiated antiidiotypicantibodies to DIGITOXIN (in a dose of 1 tablet 3 times a day). Two weekslater the patients condition was satisfactory: the blood pressure becamestable and no manifestations of cardiac failure were observed

Potentiated antibodies to antiarrhythmic drugs.

Potentiated antibodies to DISOPYRAMIDE(α-[2-[bis(1-methylethyl)amino]ethyl]-α-phenyl-2-pyridine acetamide).

I. Patient S., aged 35, complained of restlessness and tachycardia. Theoral intake of a C200 dilution of potentiated monoclonal antibodies toRYTHMILEN (DISOPYRAMIDE)(α-[2-[bis(1-methylethyl)amino]ethyl]-α-phenyl-2-pyridine acetamide) ina dose of 1 tablet 2 times a day was prescribed. At the new examinationthe patient presented no complaints for tachycardia.

Potentiated antibodies to rhythmonorm.

J. Patient Zh., aged 45, has been taking RHYTHMONORM (Propaphenone)(2[2-hydroxy-3-(propylamino)propoxy]-3-phenyl-propiophen-one), anantiarrhythmic drug of the IC class) in a dose of 150 mg 3 times a dayfor ventricular extrasystoles. The planned blood test revealedleukopenia (3.8×10³/μl) and thrombocytopenia (170×10³/μl). Rhythmonormwas discontinued. The administration of a C50 dilution of potentiatedantibodies to PROPAPHENONE in a dose of 1 tablet in the morning within10 days resulted in the normalization of the patients blood picture withpreserved antiarrhythmic effect.

Potentiated antibodies to SOTALOL(N-[4-[1-hydroxy-2-[(1-methylethyl)amino]ethyl]phenyl]methanesulfonamide).

K. Patient D., aged 28, complained of night episodes of pulseintermittence, mild pain in the left part of her thorax.Electrocardiography revealed no organic lesions of the myocardium. Afterthe preceding therapy had been cancelled, the patient started the oralintake of a C30 dilution of potentiated antibodies to SOTALOL(N-[4-[1-hydroxy-2-[(1-methylethyl)amino]ethyl]phenyl]methanesulfonamide) in a dose of 1 tablet at bedtime. During the following 10days there were no attacks of arrhythmia or pain.

Potentiated antibodies to VERAPAMIL(α-[3-[[2-(3,4-dimetoxyphenyl)ethyl]methylamino]propyl]-3,4-dimetoxy-α-(1-methylethyl)benzene-acetonitryl).

L. Patient K., aged 34, complained of headache, tachycardia, andoverfatigue. The examination revealed elevated blood pressure (140/90).The recommendation was to take nasal drops of a C200 aqueous solution ofpotentiated antibodies to VERAPAMIL(α-[3-[[2-(3,4-dimetoxyphenyl)ethyl]methylamino]propyl]-3,4-dimetoxy-α-(1-methylethyl)benzeneacetonitryl)in a dose of 0.5 ml at bedtime. The patient reported feeling better, hisblood pressure dropped to the normal level after two days of thetreatment. It was recommended to continue the course of treatment.

M. Patient Z., aged 55, with an established diagnosis of ischemic heartdisease, angina of effort, atrial extrasystoles, and tachycardia (90beats/min) had been taking 240 mg of ISOPTIN daily in a dose of 1 tablet3 times a day. The patient complained of constipation not associatedwith the regimen faults or diet changes. The intake of potentiatedantibodies to ISOPTIN LM 50 in a dose of 1 tablet 2 times a day resultedin the normalization of the bowel function without interfering with thebasic therapeutic effect of ISOPTIN. Later on, the dose of ISOPTIN wasgradually reduced and finally ISOPTIN was discontinued. The patientscondition remained satisfactory for two months against the background oftherapy with antibodies.

N. Patient D., aged 63, with the diagnosis of progressive chroniccardiac failure was treated at the cardiology unit of a clinicalhospital (intravenous infusion of 30 mg of MILRINONE daily in a dose of10 ml 3 times a day). As the patient's myocardial contractive capacityand hemodynamic indices were gradually improving, there appearedcomplaints of heartache. ECG revealed signs of myocardial ischemia. Thetreatment with a C12 dilution of potentiated antibodies to MILRINONE ina-dose of 1 tablet 3 times a day was started. Heartache disappeared, theECG pattern returned to normal, and the treatment with MILRINONE wascontinued. Gradually the preparation was discontinued and the patientwas switched to the treatment with antibodies alone in a dose of 1tablet a day. The patients condition is satisfactory.

O. Patient S., aged 58, had been taking MILRINONE for 1.5 years forchronic cardiac failure. In the course of the period of treatment thedaily dose had to be increased from 10 to 30 mg because of thedeveloping resistance to the preparation. After the prescription of aC30 dilution of potentiated antibodies to the enzyme PHOSPHODIESTERASEin a dose of 1 sublingual tablet once a day to be taken in the morningthe patients condition markedly improved: the ECG signs of myocardialoverload and ischemia became less pronounced and peripheral edemadisappeared. Three months of a regular intake of potentiated antibodiesmade it possible to reduce the daily dose of MILRINONE to 10 mg.

Potentiated antibodies to CORDARON.

P. Patient S., aged 50, had been suffering from stable angina of effortwith paroxysms of ciliary arrhythmia for 2 years. From the onset of hisillness the patient had been taking CORDARON in a dose of 600 mg a day(3 tablets). After a year of the treatment an increase in the frequencyof paroxysms of ciliary arrhythmia was registered. Paroxysms occurredevery day; an increase in the dose of CORDARON as well as theadministration of other antiarrhythmic drugs was inefficient. Nophysical or emotional strain accounted for the paroxysms; the paroxysmscease spontaneously. This condition seemed indicative of a thyroidfunction disorder; the patient was examined by an endocrinologist whoestablished the diagnosis of thyrotoxicosis of a moderate severity. Thepatient's thyroid profile looked as follows: TTH 1.29 mlU/I (the normalrange is 0.45-6.2), total T4 180.3 nmol/l (the normal range is 39-155),T33.2 nmol/l (the normal range is 1.2-3.1). The treatment with a C24dilution of potentiated antibodies to CORDARON in a dose of 1 tablet 3times a day was started. Within a month the euthyroid state wasachieved. Now the patient takes CORDARON in a dose of 100 mg a day (¼ ofa tablet 2 times a day), paroxysms of ciliary arrhythmia are rare (aboutonce a week).

EXAMPLE 32 Potentiated Antibodies to Hypocholesterolemic Drugs

Potentiated antibodies to PROBUCOL.

A. Patient K., aged 62, with the diagnosis of-coronary sclerosis, anginaof effort, and hypercholesterolemia had been taking PROBUCOL for 2months along with antianginal drugs (in a dose of 500 mg 2 times a-dayat mealtime). The patient complained of dyspepsia, meteorism in thefirst place, the onset of which dated back to one month after he hadstarted taking the preparation. The administration of a C30 dilution ofpotentiated antibodies to PROBUCOL in a dose of 1 tablet a daycontrolled the patients intestinal disorders. The daily dose of PROBUCOLwas reduced by 50%.

Potentiated antibodies to NICOTINIC ACID.

B. Patient L., aged 58, had been taking NICOTINIC ACID in a dose of 4.0g a day for atherosclerosis of peripheral vessels (especially pronouncedin the lower extremities). The patient complains of hot flashes andredness of the face. The intake of a C12 dilution of potentiatedantibodies to nicotinic acid in a-dose of 1 tablet 3 times a dayimproved the patients tolerance of the preparation and made it possibleto reduce its dose to 1.0 g a day.

Potentiated antibodies to PRAVASTATIN.

C. Patient F., aged 57, suffered from ischemic heart disease and primaryhypercholesterolemia. He had been taking PRAVASTATIN for 3 months in adose of 20 mg at bedtime along with NITROGLYCEROL (up to 5-6 tablets aday for angina attacks). In the course of the last 10-15 days he noticedthe development of muscular weakness. The biochemical analysis of thepatients blood revealed transaminase levels elevated to the upper bound(ALT 50 IU/l, AST 45 IU/l). The administration of a C200 dilution ofpotentiated antibodies to PRAVASTATIN in a dose of 1 tablet once a dayresulted in the improvement of the patients condition of health, hisblood transaminase level lowered (ALT 26 IU/l, AST 21 IU/l). Anginaattacks became less frequent and the patients intake of nitroglyceroltablets reduced to 1-2 tablets a day.

Potentiated antibodies to ETOFIBRATE.

D. Patient P., aged 55, with an established diagnosis of ischemic heartdisease and hypercholestrolemia had been taking ETOFIBRATE (in a dose of500 mg once a day) following his physician's advice. The patient statedthat after a month of the treatment with this preparation he began tosuffer from abdominal pain and meteorism. The intake of a C30 dilutionof potentiated antibodies to ETOFIBRATE in a dose of 1 tablet a dayresulted in the normalization of the patients condition. The dose ofETOFIBRATE was reduced by 50%. The patients lipid metabolism indicesremained within normal limits.

Potentiated antibodies to ORLISTATE.

E. Patient O., aged 59, suffered from diabetes mellitus, Type 2, andobesity (height 160 cm, body weight 100 kg) and had been taking 120 mgof ORLISTATE (the inhibitor of gastric lipases) 3 times a day at meals.Within several months of the treatment combined with low-calorie dietthe patient body weight decreased by 7 kg; however, the patientcomplained of poor feeling, which was manifested by meteorism andimperative rectal tenesmus. The prescription of a C200 dilution ofpotentiated polyclonal antibodies to ORLISTATE in a dose of 1 tablet aday improved the patient's tolerance of the preparation, decreased herblood sugar level, and made it possible to reduce the dose of insulin.

EXAMPLE 33 Potentiated Antibodies to Antitumor Drugs

Potentiated antibodies to DOXORUBICIN[(8S-cis)-10-[(3-amino-2,3,6-dideoxy-α-L-lyxohexo-pyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphtacenedione].

A. Patient P., aged 61, had been receiving a course of chemotherapy withDOXORUBICIN[(8S-cis)-10-[(3-amino-2,3,6-dideoxy-α-L-lyxohexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphtacenedione]for lung cancer but had to stop taking the medication because of nauseaand vomiting. The prescription was to combine the administration of thecytostatic drug with the oral intake of a C6 solution of potentiatedmonoclonal antibodies to DOXORUBICIN. As a result the nausea subsided,which made it possible to continue chemotherapy. Later on, DOXORUBICINwas discontinued and the patient was put on potentiated anti-bodiesalone. The patient is feeling well and X-ray findings show the arrest oftumor growth.

Potentiated antibodies to CISPLATIN (cis-diaminodichloriplatinum).

B. Patient D., aged 57, complained of cramps in her lower extremitiesduring the process of chemotherapy with CISPLATIN for ovarian cancer. AC12 dilution of potentiated monoclonal antibodies tocis-diaminodichlorplatinum in a dose of 2 ml intramuscularly once a daywas prescribed. This drug made it possible not only to control crampsand improve the patient's tolerance of cisplatin but also to reduce thedose of the latter by 50%.

Potentiated antibodies to METHOTREXATE(N-[4-[[(2,4-diamino-6-pteridinyl)methyl]methylamino]benzoyl]-glutamicacid).

C. Patient P., aged 9, was admitted to hospital for acute lymphoblasticleucosis. In the course of chemotherapy with METHOTREXATE the patientstarted complaining of severe headaches and nausea. The treatment with aD12 dilution of a potentiated antiserum to METHOTREXATE in a dose of 1tablet 2 times a day was begun. Two days later, with continuedchemotherapy, the patient reported that his headaches disappeared andnausea subsided. He kept taking the potentiated preparation. Two monthslater the patients condition was satisfactory and METHOTREXATE wasdiscontinued. Four months later, against the background of continuedmonotherapy with antibodies, the patient's lymphogram was close tonormal.

Potentiated antibodies to THALIDOMIDE.

D. Patient U., aged 42, suffered from multiple myeloma. Two bone marrowtransplantations resulted in short remissions. The third transplantationdid not lead to a remission; the blood MIG (myeloma immunoglobulin, aprotein marker of tumor cells) level was rising. The treatment withTHALIDOMIDE made it possible to achieve stable remission and thedepression of the blood MIG level; however the patient startedcomplaining of weakness, drowsiness constipation, and numbness sensationin his extremities. It was suggested to use the intranasaladministration of a C30 dilution of potentiated antibodies toTHALIDOMIDE in a dose of 1 ml 3 times a day as additional treatment.After a week of treatment with antibodies the patient started feelingbetter, no signs of the progressive course of his myeloma were observed,and the blood MIG level kept falling dramatically.

Potentiated antibodies to VERAPAMIL.

E. Patient Sh., aged 29, with an established diagnosis of small-cellcarcinoma of his left lung was going through a course of chemotherapywith cisplatin and methotrexate. The patient was also taking VERAPAMIL(a calcium channel blocker) in order to enhance the tumor cellsensitivity to the treatment. After a month of treatment, there appearedsymptoms of cancer progression. Added to the treatment protocol was theintake of a C200 dilution of potentiated anti-bodies to VERAPAMIL in adose of 1 tablet-a day. The patient started feeling better and his X-rayimage showed the arrest of tumor progression.

POTENTIATED ANTIBODIES to TOPOISOMERASE II

F. Patient T., aged 40, with an established diagnosis of lung carcinomaunderwent two courses of treatment with CISPLATIN and ETOPOSIDE, afterwhich clinical and X-ray findings revealed the tumor's primaryresistance to antitumor drugs. The third course of the treatment withcytostatic drugs was combined with the administration of a C30 dilutionof potentiated antibodies to TOPOISOMERASE II in a dose of 1 sublingualtablet once a day. The patient started feeling better and X-ray patternsrevealed the arrest of tumor progression.

Potentiated antibodies to PROSPIDINE.

G. Patient R. aged 37 was undergoing hospital treatment with PROSPIDINE(300 mg in the form of intramuscular injections 3 times a week) asmonochemotherapy for T lymphoma of the skin. A decrease in the area ofskin lesions (by 30%) along with improved laboratory test data allowedthe treatment to be regarded as efficient; however, there was no furtherprogress in the patient's condition. The treatment was supplemented witha C200 dilution of potentiated antibodies to PROSPIDINE in a dose of 1tablet a day. The area of skin lesions reduced by another 40%.

Potentiated antibodies to hormone antagonists

TAMOXIFEN((Z)-2-[4-(1,2-diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine).

H. Patient I., aged 47, was taking a course of chemotherapy withTAMOXIFEN(Z)-2-[4-(1,2-diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine) forbreast cancer; she complained of dizziness and nausea. The intranasaladministration of 0.5 ml of a C30 aqueous solution of potentiatedmonoclonal antibodies to TAMOXIFEN 3 times a day was prescribed. Thepatient's nausea subsided to a bearable level.

Potentiated antibodies to FLUTAMIDE(2-methyl-N[4-nitro-3-(trifluormethyl)phenyl]propanamide).

I. Patient U., aged 41, complained of fatigue and the loss of libido andpotency. The administration (in the form of intranasal drops at bedtime)of 0.5 ml of a C12 solution of a potentiated antiserum to FLUTAMIDE(2-methyl-N[4-nitro-3-(trifluormethyl)phenyl]propanamide). After 10 daysof the treatment the patient stated the improvement of his ability towork and sexual activity. It was recommended to continue the course oftreatment.

EXAMPLE 34 Potentiated Antibodies to Regulators of the Blood CoagulationProcess

Potentiated antibodies to HEPARIN (mucopolysaccharide of a polysulfuricacid ester).

A. Patient M., aged 59, complained of superficial pains in her lowerextremities. The diagnosis of trombophlebitis was established; aqueouscompresses with a D6 solution of a potentiated antiserum to heparin atbedtime were recommended. After 5 procedures the pain and local rednesssubsided.

Potentiated antibodies to TICLOPIDINE(5-[2-chlorophenyl)methyl]-4,5,6,7-tetrahydrothieno[3,2-c]pyridine).

B. Patient K., aged 63, complained of moderate heartaches. The diagnosisof ischemic heart disease was made. The oral intake (at bedtime) of 20ml of a C30 potentiated solution of polyclonal antibodies to TICLOPIDINE(5-[2-chlorophenyl)methyl]-4,5,6,7-tetrahydrothieno[3,2-c]pyridine) C30in a dose of 1 tablet 3 times a day was prescribed. After 3 months ofthe treatment no worsening of the disease was observed. The conclusionwas drawn about the efficiency of the potentiated preparation for theprevention of ischemic heart disease.

EXAMPLE 35 Potentiated Antibodies to Hormonal Agents

Potentiated antibodies to INSULIN.

A. Patient R., aged 45, with an established diagnosis of diabetesmellitus Type 1 complained of ulcer of the skin integument of his lowerextremities. Local rubbing with a C30 dilution of a 30% alcoholicsolution of an antiserum to insulin was included into the scheme ofcombined therapy. Epithelization of skin integument lesions wasachieved.

B. Patient D., aged 52, with an established diagnosis of diabetesmellitus Type 2 had an excessive body weight. His fasting blood glucoselevel was 10 mmol/l. The glucose level correction could not be achievedby diet and synthetic antihyperglycemic agents. Within 3 months thedaily dose of insulin increased from 5 to 25 units. The treatment with aC200 dilation of potentiated monoclonal antiidiotypic antibodies toinsulin in a dose of 1 tablet a day was started. Two weeks later thepatient's sensitivity to insulin increased; the dose of insulin wasreduced to units, the fasting blood glucose level reached 5 mmol/l.After 2 months of the treatment insulin was discontinued and the patientwas switched to therapy with antibodies alone.

C. Patient I., aged 48, suffered from a severe form of diabetes mellituswith a high degree of insulin resistance (the patient needed up to 128units a day). The treatment with a C30 dilution of a potentiatedantiserum to the insulin-like growth factor in a dose of 1 tablet 3times a day resulted in a marked improvement of the patient's condition.His blood-glucose level dropped to 16 mmol/l. The daily dose of insulinwas reduced by 50%.

Potentiated antibodies to ESTRADIOL.

D. Patient B., aged 34, was admitted to the neurology department of aclinical hospital with complaints of rapid uncontrollable movements inher right extremities. These symptoms developed after a common cold. Thepatient gave no history of rheumatic fever. At the time of admission thepatient was pregnant for the second time (the 21^(st)-22^(nd) week); shesuffered from early gestosis; there had been no complications in thecourse of her first pregnancy. Before deciding to have another baby thepatient had been taking oral contraceptives. The patient was slightlyeuphoric. The memory and intellect were unimpaired. Her arterial bloodpressure was 120/80 mm Hg. Hyperkinesias of her right extremities,predominantly in her arm and hand were found. Gynecological examinationdid not reveal any indication for the termination of pregnancy. Thetreatment with a C200-dilution of a potentiated form of antibodies toESTRADIOL in a dose of 1 tablet a day was started; a week later thesymptoms of hyperkinesia disappeared. The patient had an uncomplicateddelivery at term; her baby was in good health.

Potentiated antibodies to GLUCAGON.

Patient T., aged 64, complained of bradycardia and arterial hypotensionupon admission; she had been taking ATENOLOL. The oral administration ofa C12 dilution of potentiated polyclonal antibodies to GLUCAGON in adose of 1 tablet 3 times a day was prescribed. Within 24 hours thenormalization of the cardiac rhythm and arterial pressure was achieved.

Potentiated antibodies to TRIIODOTHYRONINE (LIOTHYRONINE)(O-(4-hydroxy-3-c-iodophenyl)-3,5-diiodo-L-thyrosine).

E. Patient D., aged 36, complained of tachycardia and heartaches. Theexamination revealed no organic disorders. The oral intake of a C12dilution of potentiated polyclonal antibodies to TRIIODOTHYRONINE(O-(4-hydroxy-3-c-iodophenyl)-3,5-diiodo-L-thyrosine) in a dose of 1tablet 3 times a day was prescribed. After 5 days of the treatment thenormalization of cardiac rhythm and the disappearance of pain wereachieved.

Potentiated antibodies to CALCITONIN.

F. Patient I., aged 58, complained of pain in her tubular bones and softtissues of her extremities. The examination confirmed the diagnosis ofosteoporosis. The intranasal administration of 0.5 ml a C24 dilution ofa potentiated monospecific antiserum to CALCITONIN twice a day wasprescribed within the framework of combined therapy. Three days laterthe patient started feeling better and reported the lessening of pain.

Potentiated antibodies to the SOMATOTROPIC HORMONE.

G. Patient Ch., aged 56, had been taking a course of treatment forobesity. Because of the oral administration of a C15 dilution ofpotentiated monoclonal antibodies to the somatotropic hormone in a doseof 1 tablet 3 times a day together with a diet the patient had lost 4kilograms within 10 days; the dieting became easier.

Potentiated antibodies to STEROID HORMONES.

Potentiated antibodies to HYDROCORTISONE(11β)-11,17,21-trihydroxypregn-4-ene-3,20-dione).

I. Patient Ts., aged 29, a welder by profession complained of sharp painin his eyes. Twice doses of eye drops containing a C12 aqueous solutionof a potentiated antiserum to HYDROCORTISONE(11β)-11,17,21-trihydroxypregn-4-ene-3,20-dione) made it possible toeliminate painful sensations within 24 hours.

Potentiated antibodies to DEXAMETHASONE(11β,16α)-9-fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione).

J. Patient D., aged 39, complained of itching in his nasopharynx. Afterintranasal administration of 1 ml of a C12 dilution of a potentiatedsolution of monoclonal antibodies to DEXAMETHASONE(11β,16α)-9-fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione)itching disappeared.

Potentiated antibodies to TESTOSTERONE((17β)-17-hydroxyandrost-4-en-3-one).

K. Patient A., aged 41, complained of the lowering of potency. Theexamination revealed a moderate degree of obesity and no organic lesionsof the central nervous system. A course of treatment with a C6 dilutionof potentiated monoclonal antibodies to TESTOSTERONE to be taken bymouth in a dose of 1 tablet 3 times a day was proposed. At his nextvisit to the physician four weeks later the patient stated that hissexual performance improved and sexual activity enhanced. The patienthad lost 5 kg; he tolerated well his food regimen under the conditionsof the preparation intake. It was recommended to continue the course oftreatment.

EXAMPLE 36 Potentiated Antibodies to Nervous System Mediators

Potentiated antibodies to ACETYLCHOLINE(2-(acetyloxy)-N,N,N-trimethylethaneaminium).

A. Patient Yu., aged 58, complained of constipation. The intranasaladministration of 0.5 ml of a C50 dilution of a potentiated solution ofantibodies to ACETYLCHOLINE (2-(acetyloxy)-N,N,N-trimethylethaneaminium)4 times a day was recommended. The stool was back to normal 24 hoursafter the intake of the preparation.

Potentiated antibodies to NORADERNALINE.

B. Patient D., aged 71, complained of dizziness and bradycardia. Theexamination revealed hypotension (100/65 mm Hg). The oral intake of 10ml of an antiserum to noradrenaline in a potency of C14, 3 times a daywas prescribed. At his next visit to the physician 6 days later thepatient reported feeling better and not suffering from dizzinessanymore; his blood pressure was 110/75 mm Hg. It was recommended tocontinue the course of treatment.

Potentiated antibodies to DOPAMINE.

C. Patient L., aged 69, complained of tremor and gait disorders. Thepatient had had a long-time history of treatment with neuroleptics forschizophrenia. The treatment was supplemented with a C15 dilution ofpotentiated polyclonal antibodies to dopamine (oral intake, 1 tablet 3times a day). Within 4 days the tremor disappeared and no neurolepticmanifestations were observed.

Potentiated antibodies to SEROTONIN (5-hydroxytriptamine).

D. Patient G., aged 41, complained of the worsening of mood and apathy.The intake of a C1000 dilution of a potentiated solution of monoclonalantibodies to (serotonin) in the form of drops in a dose of 1 ml twice aday was proposed. Seven days later the patient reported the improvementof mood and the enhanced motivation to labor. It was recommended tocontinue the course of treatment.

Potentiated antibodies to ASPARTIC ACID (L-aspartic acid).

E. Patient N., aged 75, complained of tremor of extremities. Theexamination revealed no organic lesions of the nervous system. The oralintake of a C200 dilution of a potentiated solution of antibodies toaspartic acid in a dose of 1 tablet 3 times a day was recommended. A newexamination two days later showed the absence of tremor.

Potentiated antibodies to GLUTAMIC ACID (L-glutamic acid).

F. Patient M., aged 29, complained of cramps in the lower extremitiesduring sleep. The administration of potentiated polyclonal antibodies toL-glutamic acid in a dose of 1 tablet by mouth at bedtime resulted in adecrease in the frequency and intensity of convulsions.

Potentiated antibodies to GLYCINE.

G. Patient P., aged 58, complained of restlessness and sleepingdisorders. The oral intake of a C1000 dilution of potentiated antibodiesto GLYCINE in a dose of 1 tablet at bedtime was recommended; within twodays the patients sleep became normal.

EXAMPLE 37 Potentiated Antibodies to Mediators of Inflammation andAllergy

Potentiated antibodies to PROSTAGLANDINS.

Potentiated antibodies to MISOPROSTOL (methyl ester of(11α,13E)-(+−)-11,16-dihydroxy-methyl-9-oxoprost-13-en-1-ic acid).

A. Patient K., aged 41, complained of pain in the epigastic area aftermeals. The oral intake of a C50 dilution of a potentiated solution ofpolyclonal antibodies to MISOPROSTOL (methyl ester of(11α,13E)-(+−)-11,16-dihydroxy-methyl-9-oxoprost-13-en-1-ic acid) in adose of 1 tablet before meals was recommended. At his new visit to thephysician seven days later the patient reported the elimination of pain.

Potentiated antibodies to KININS.

B. Potentiated antibodies to BRADYKININ.

Patient N., aged 15, complained of dry cough. The administration ofpotentiated monoclonal antibodies to bradykinin in the form of nasaldrops in a dose of 0.5 ml 3 times a day resulted in the disappearance ofcough within 2 days.

Potentiated antibodies to HISTAMINE (1H-imidazole-4-ethanamine).

C. Patient Ts., aged 27, complained of severe itching of insect bites.Within the framework of combined therapy compresses with a C30 solutionof potentiated antibodies to histamine were applied to the sites oflesions. The next day the redness subsided and the itching disappeared.

EXAMPLE 38 Potentiated Antibodies to Vitamins, Substances withVitamin-Like Action, and Bioflavonoids

A. Patient A., aged 51, had been taking rather large doses of ascorbicacid (5-6 g daily) with health-improvement purposes following hisfriends' advice. He was admitted to hospital with an attack of renalcolic. The pain was controlled with spasmolytic drugs and alkalinesolutions. Laboratory blood tests showed high glucose content (9 mmol/l,the normal range being from 3.3 to 5.5 mmol/l). The patient had neverconsulted endocrinologist and had no family history of diabetes;therefore, the toxic effect of high doses of ascorbic acid upon thepancreas was suggested as the cause of the patients elevated blood sugarcontent. The treatment with potentiated antibodies to ascorbic acid in adose of 1 tablet 3 times a day was started. Within two weeks the fastingblood glucose content dropped to 6 mmol/l.

Potentiated antibodies to THIAMINE(3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-5-(2-hydroxyethyl)-4-methylthiazoliumchloride).

B. Patient V., aged 57, complained of pain in her left thigh. Theexamination confirmed the diagnosis of neuralgia. A C200 dilution of apotentiated solution of monoclonal antibodies to THIAMINE(3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-5-(2-hydroxyethyl)-4-methylthiazoliumchloride) in a dose of 1 tablet twice a day was recommended. After 6days of the treatment the lessening of the pain intensity was achieved.A conclusion about the efficiency of such therapy was drawn.

Potentiated antibodies to NICOTINIC ACID (3-pyridinecarboxylic acid).

C. Patient R., aged 48, complained of hot flashes and tachycardia afterthe intake of nicotinic acid she had been receiving for atherosclerosis.The oral intake of a C30 dilution of a potentiated solution ofmonoclonal antibodies to 3-pyridinecarboxylic acid in a dose of 1 tablettwice a day was recommended. The patient noticed the subsidence of hertachycardia, which allowed the antihypercholesterolemic therapy to becontinued.

Potentiated antibodies to TROXERUTIN(2-[3,4-(bis(2-hydroxyethoxy)phenyl]-3-[[6-O-(6-deoxy-α-L-mannosopyranoz-yl)-β-D-glucopyranozyl]oxy]-5-hydroxy-7-(2-hydroxyethoxy)-4H-1-benzopyranone-4).

D. Patient U., aged 42, complained of pain after she had bruised herthigh. The examination revealed a large hematoma. Compresses with a C6dilution of an aqueous solution of a potentiated antiserum to TROXERUTINwere recommended. A new examination two days later showed the shrinkingof the hematoma; the patient felt no pain.

Potentiated antibodies to DIHYDROERGOCRISTINE.

E. Patient K., aged 29, had been taking 1 lozenge of ANAVENOL (thepreparation composed of an α-adrenolytic agent DIHYDROERGOCRISTINE,ESCULINE, and RUTOZIDE) 3 times a day for varicose veins in her legsdeveloped during pregnancy and the postpartum period. The edema andheavy feeling in the legs were lessening but the patient startedcomplaining of headaches and dizziness. Anavenol was discontinued. Thetreatment with a C30 dilution of potentiated antibodies todihydroergocristine in a dose of 1 tablet twice a day was begun. Thepatient's condition of health kept improving, headaches and dizzinessdisappeared. Two months later a marked regression of varicosity wasregistered.

Potentiated antibodies to DETRALEX bioflavonoid (contains a combinationof diosmine and hesperedin).

F. Patient V., aged 42, an operation nurse, had been suffering fromvaricose veins in her legs for 5 years. Following her doctor'srecommendations, she started taking DETRALEX (1 tablet twice a day). Shecomplained of dyspepsia not associated with diet faults. The treatmentwith a C30 dilution of potentiated antibodies to each componentalternately (every other day) in a dose of 1 tablet daily was initiated.The patient started feeling much better after one week of the intake ofthe antibodies. Six weeks later no symptoms of varicose veins were seen.

Potentiated antibodies to VITAMIN A.(trans-9,13-dimethyl-7-(1,1,5-trimethylcyclohexen-5-yl-6)-nonatetraen-7,9,11,13-ol).

G. Patient K., aged 26, complained of headache, running nose andartralgia. In order to raise the patients immunity, the oral intake of aC200 dilution of a potentiated antiserum to VITAMIN A(trans-9,13-dimethyl-7-(1,1,5-trimethylcyclohexen-5-yl-6)-nonatetraen-7,9,11,13-ol)in a dose of 1 tablet a day was prescribed. At his next visit three dayslater the patient reported feeling well.

Potentiated antibodies to VITAMIN D (ERGOCALCIFEROL)(5Z,7E,22E)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol).

H. Patient N., aged 55, complained of pain in his hands not associatedwith physical strain and cramps in his lower extremities. Therecommendation was: the intake of a C200 dilution of potentiatedsolution of an antiserum to VITAMIN D (ERGOCALCIFEROL)(5Z,7E,22E)-9,10-secoergosta-5,7,10(19),22-tetraen-3-ol) in a dose of 1tablet 2 times a day in combination with preparations of calcium. Afterthree weeks of the therapy the lessening of pain and the disappearanceof convulsive reactions were observed. It was recommended to continuethe course of treatment.

Potentiated antibodies to VITAMIN E(3,4-dihydro-2,5,7,8,-tetramethyl-2-(4,8,12,trimethyltridecyl)-2H-1-benzopyranolacetate).

I. Patient A., aged 43, complained of fatigability and muscle weakness.After a weeklong course of treatment with a C30 dilution of potentiatedmonoclonal antibodies to VITAMIN E(3,4-dihydro-2,5,7,8,-tetramethyl-2-(4,8,12,-trimethyltridecyl)-2H-1-benzopyranolacetate) in a dose of 1 tablet 3 times a day the patient stated anincrease in his ability to work and the improvement of mood.

EXAMPLE 39 Potentiated Antibodies to Immunomodulators and Cytokines

Potentiated antibodies to INTERFERON.

A. Patient P., aged 34, complained of rhinitis and pain in hisnasopharynx. The diagnosis of acute respiratory viral infection wasestablished. A double administration of intranasal drops of apotentiated C12 aqueous solution of monoclonal antibodies toγ-interferon resulted in the normalization of the patient's condition ofhealth within two days. A conclusion was made that the antibodiesfeatured the antiviral effect.

Potentiated antibodies to interleukins.

Potentiated antibodies to ALDESLEUKIN (INTERLEUKIN 2)

B. Patient M., aged 42, had been running course of treatment for theexacerbation of chronic bronchitis. The oral intake of a C30 dilution ofpotentiated monoclonal antibodies to INTERLEUKIN 2 in a dose of 1 tablet3 times a day resulted in the normalization of the body temperaturethree days after the beginning of the treatment with the homeopathicpreparation. The recommendation was to take the preparation in a dose of1 tablet once a day for three months. Catamnesis: no exacerbations ofchronic bronchitis occurred during 8 months of medical observation. Aconclusion was made that the antibodies possessed an immunity boostingeffect.

Potentiated antibodies to COLONY-STIMULATING FACTORS.

C. Patient L., aged 23, complained of dizziness. He had a long (20 days)history of the intake of baralgin containing a pyrazolone derivativewith a hemopoiesis-suppressing effect. The oral intake of a C200dilution of potentiated polyclonal antibodies to FILGRASTIM(COLONY-STIMULATING FACTOR) in a dose of 1 tablet 3 times a day wasrecommended; this made it possible to achieve normal counts ofneutrophiles and erythrocytes within 6 days after the beginning oftreatment. Conclusion: the antibodies possessed a hemopoietic effect.

Potentiated antibodies to LEVAMIZOL.((S)-2,3,5,6-tetrahydro-5-phenylmidazo[2,1-b]thiazole).

D. Patient K., aged 41, was hospitalized with an established diagnosisof maxillary sinusitis. The administration of a C12 dilution ofpotentiated monoclonal antibodies to LEVAMIZOL((S)-2,3,5,6-tetrahydro-5-phenylmidazo[2,1-b]thiazole) in the form ofnasal drops in a dose of 0.5 ml twice a day made it possible to controlheadache and to return the body temperature to the normal level withinthree days. It was the immunostimulating effect of potentiatedantibodies that accounted for such results.

E. Patient P., aged 53, suffered from the exacerbation of herhypertensive disease; the blood pressure reached 180/100 mm Hg. As sheused to take DIBAZOL as part of her antihypertension treatment, therewas made a suggestion to start treatment with a C30 dilution ofpotentiated polyclonal antibodies to DIBAZOL in a dose of 1 tablet twicea day. Within three days her blood pressure dropped to 150/80 mm Hg. Thetreatment with antibodies was continued. Despite the fact that there wasan epidemic of flu in the city, to which all the members of the patientsfamily succumbed, the patient never developed any symptoms of viralrespiratory infection. A conclusion was drawn about the hypotensive andimmunostimulating effects of the antibodies.

Potentiated antibodies to immunodepressant drugs.

F. Patient D., aged 27, complained of redness and itching of her handsafter a contact with a synthetic detergent. Her condition was diagnosedas allergic dermatitis. The oral intake of a C200 dilution of ahomeopathic solution of monoclonal antibodies to CYCLOSPORIN in a doseof 1 tablet twice a day lessened the severity of the allergic reactionwithin 24 hours.

G. Patient A., aged 28, had been staying at hospital for basicantirheumatic therapy-resistant rheumatoid arthritis. The patient hadbeen treated with CYCLOSPORIN A (CsA) (2.5 mg/kg per diem) for 4 monthswith good therapeutic effect. A routine blood test showed an elevatedcreatinine level; the patients blood pressure was raising in the courseof the last week (160/90 mm Hg). The danger of the exacerbation ofarthritis and the inefficiency of other medications precludedcancellation of treatment with CsA. The dose of CsA was reduced to 1.5mg/kg per diem and a C200 dilution of potentiated antibodies to CsA wasprescribed in a dose of 1 tablet twice a day. After a week of thetreatment the creatinine content went back to normal, the blood pressuredropped to 120/75 mm Hg. The stable antirheumatic effect of CsApersisted along with the patients good tolerance of it. Later CsA wasdiscontinued. The intake of potentiated anti-bodies was continued in adose of 1 tablet every day. Catamnesis 6 months later: rheumatoidarthritis in the phase of remission.

H. Patient L., aged 47, complained of lumbar pain. After the diagnosisof lumbosacral radiculitis had been established, a recommendation wasmade: the oral intake of a C12 dilution of polyclonal antibodies toCHONDROITIN SULFATE in a dose of 1 tablet 3 times a day along withconventional anti-inflammatory drugs. After two days of the treatmentthe pain syndrome subsided. Monotherapy with antibodies made it possibleto begin to control the manifestations of radiculopathy within 7 days.

I. Patient O., aged 40, had been participating in the elimination of theconsequences of the Chernobyl catastrophe; he suffered from radiationcataract of both eyes. The patient used to take AZAPENTACENE (2 dropsinto both eyes 5 times a day) to good effect; however he complained tothe attending oculist of an itching and burning sensation in hiseyelids. The suggestion was to discontinue the administration of thepreparation temporarily and to use a D12 dilution of anti-bodies toAZAPENTACENE in a dose of 1 tablet twice a day. When the irritation ofthe patient's eyelids had subsided, the treatment with potentiatedantibodies was successfully continued.

EXAMPLE 40 Potentiated Antibodies to Antibiotics and Antiparasite Drugs

Potentiated antibodies to CIPROFLOXACIN(1-cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-7-(1-piperazinyl)-3-quinolinecarboxylicacid).

A. Patient Ts., aged 26, complained of cough and pain in hisnasopharynx. Physical examination showed a rise in the body temperatureto 37.1° C. After two days of the intake of a solution of potentiatedantibodies to CIPROFLOXACIN(1-cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-7-(1-piperazinyl)-3-quinolinecarboxylicacid) in a dose of 10 drops 3 times a day the patients conditionnormalized and the body temperature dropped to 36.7° C.

Potentiated antibodies to METRONIDAZOLE(2-methyl-5-nitro-1H-imidazole-1-ethanol).

B. Patient A., aged 32, complained of nausea after metronidazol intake.The additional administration a of C12 dilution of potentiatedmonoclonal antibodies to 2-methyl-5-nitro-1H-imidazole-1-ethanol in adose of 1 tablet 3 times a day made it possible to eliminate nausea andcontinue the treatment.

C. Potentiated antibodies to CEFEPIM([[7-[[(2-amino-4-thiazolyl)(metoxyimino)acetyl]amino]-2-carboxy-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-en-3-yl]methyl]-1-methylpyrrolidiniumhydroxide).

Patient E., aged 36, complained of pain in his knee joints andtonsillitis. The diagnosis of rheumatoid arthritis was establishedearlier; however, concomitant duodenal ulcer precluded theadministration of anti-inflammatory drugs. The recommendation was totake drops of a solution (a D24 dilution) of an antiserum to theantibiotic CEFEPIM([[7-([[2-amino-4-thiazolyl)(metoxyimino)acetyl]amino]-2-carboxy-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-en-3-yl]methyl]-1-methylpyrrolidiniumhydroxide) 3 times a day. Five days later the inflammatory reactionsubsided and tonsillitis disappeared.

D. Patient Zh., aged 33, was directed to the proctology unit of aclinical hospital with an established diagnosis of perianal abscess.Within the framework of therapy the patient was receiving AMOXYCLAV (acombination of semisynthetic penicillin amoxycillin and clavulonic acid,an inhibitor of β-lactamases), 1 tablet 3 times a day. The patient usedto take various antibiotics on his own initiative and without system,including phenoxymethylpenicillin. Along with the amelioration of hisgeneral condition (the lowering of the body temperature, the lesseningof pain, and the reduction of the white blood count), the patientstarted complaining of nausea. Following his doctor's advice, thepatient began to take AMOXYCLAV at meals; however, nausea persisted. A7-days' course of the treatment with a C6 dilution of potentiatedantibodies to 6-aminopenicillanic acid (common for all penicillins) in adose of 1 tablet 3 times a day was carried out. The tolerance of thepreparation improved; the patient presented no complaints, noindications for surgical treatment were seen; as the blood count and thebody temperature were back to normal, the patient was discharged fromhospital under local polyclinic observation. Recommendations for theregimen and further treatment were given.

E. Patient V., aged 34, suffered from severe bilateral polysegmentarypneumonia with a II-III degree of respiratory failure, chronicalcoholism, chronic hepatitis, secondary immunodeficiency. The patientstarted receiving MAXINIM (cephalosporin of the IV generation) in a doseof 1.0 gram intramuscularly every 12 hours. At the 3^(rd) day of thetreatment the patient's condition ameliorated, dyspnea and coughsubsided, and the body temperature went down. However, the paint startedcomplaining of nausea, his functional liver tests showed elevated valuesof ALT and AST. The treatment protocol was completed with a C50 dilutionof potentiated antibodies to MAXINIM in a dose of 1 tablet 3 times aday. The patient's condition kept improving, the nausea disappeared, andthe ALT and AST values dropped to the upper bound of normal.

F. Patient K., aged 46, was taking RULIDE for acute prostatitis in adose of 150 mg twice a day. After three days of the treatment thesymptoms of prostatitis subsided but the patient started complaining ofdizziness and distorted smell and taste of food. The treatment with aC30 dilution of potentiated antibodies to RULIDE in a dose of 1 tablet 3times a day was started and within three days the taste and odorperception was back to normal and dizziness disappeared.

G. Patient G., aged 25, suffered from the exacerbation of chronicadnexitis after criminal abortion, polynarcomania, and secondaryimmunodeficiency. She was treated with CIPROBAY (125 mg 2 times a day).After 6 days of the treatment the patient felt better; however, shestarted having fainting spells and hot flashes. A C200 dilution ofpotentiated antibodies to CIPROBAY in a dose of 1 tablet twice a day wasprescribed. Within the days the patient's complaints disappeared, hercondition became satisfactory.

H. Patient Sh., aged 44, had been treated with CIPROFLOXACIN for theexacerbation of chronic suppurative obstructive bronchitis. The choiceof the drug had been based on the results provided by theantibioticogram; the repeated use if this medication had been givingclinical success. However, in this case no positive bronchologicaldynamics was achieved after 2 weeks of treatment. The antibiotic wasdiscontinued and the treatment with a C6 dilution of potentiatedmonoclonal antibodies to CIPROFLOXACIN in a dose of 1 tablet twice a daybegan. Within ten days all symptoms of bronchial obstructiondisappeared, no suppurative mucus was seen during bronchoscopy. Aconclusion was drawn on the anti-bacterial and anti-inflammatory effectsof potentiated antibodies.

I. Patient I., aged 42, was staying in a phthisiologic hospital with anestablished diagnosis of infiltrative tuberculosis of the upper lobe ofthe right lung in the phase of disintegration and dissemination, withbacterioexcretion. After three months of the treatment with isoniazid,rifampicin, and streptomycin positive clinical and X-ray dynamics wasachieved. However, the subsequent two months of the treatment with theantibacterial drugs did not bring any significant improvement of thepatients condition: infiltration and a cavern in the upper lobe of theright lung persisted and showed no tendency for a further reduction; therelease of bacteria persisted as well. The in vitro resistance toantibiotics was not found at the initial stage of examinations or fivemonths later. The treatment with a C200 dilution of potentiatedantibodies to ISONIAZID, RIFAMPICIN, and STREPTOMYCIN in a dose of 1tablet of each preparation daily made it possible to achieve positiveX-ray dynamics within two months; the release of bacteria stopped.

J. Patient Ch., aged 36, was staying at the infectious hospital foramebic dysentery. After four days of the administration of ORNIDAZOLE(1.0 g per diem) the patient started complaining of somnolence anddizziness. The additional treatment with a C12 dilution of potentiatedantibodies to ORNIDAZOLE in a dose of 1 tablet twice a day resulted inthe elimination of the undesirable effects within subsequent four days.

EXAMPLE 41 Potentiated Antibodies to Chelating Agents

A. Patient D., aged 44, was undergoing a course of treatment withDOXORUBICIN (75 mg administrated intravenously once in 3 weeks) at thein-patient unit of an oncological dispensary for III degree breastcancer. For the prevention of myocardiopathy the patient was receivingCARDIOXANE intravenously 30 minutes before the injection of thecytostatic drug. The patient tolerated DOXORUBICIN well enough with abackground treatment with CARDIOXANE; however, her hemoglobin leveldropped to 70 g/l. It was suggested to include the administration of aC30 dilution of potentiated antibodies to CARDIOXANE in a dose of 1tablet twice a day in the treatment protocol. Within subsequent threemonths the remission of the main disease was achieved and maintained; nosigns of cardiac failure were observed and the hemoglobin level was95-100 g/l.

EXAMPLE 42 Potentiated Antibodies to Anti-Gout Drugs

A. Patient Kh., aged 49, with the diagnosis of hypertensive disease andchronic gout had been taking 1.5 g of PROBENECIDE daily for theprevention of gout exacerbation caused by a diuretic (hypothiazide) hewas receiving for his hypertension. The patient complained of nausea,weakness and painful sensation in his gums. The treatment with a C12dilution of potentiated antibodies to PROBENECIDE in a dose of 1 tablettwice a day was started and three days later the patient started feelingbetter. The treatment with hypothiazide and PROBENECIDE was continued;the PROBENECIDE dose was reduced by 50% with no negative effect on thetherapeutic action.

B. Patient V., aged 51, had been taking (on his physician's advice)IMODIUM (LOPERAMIDE) for chronic-diarrhea caused not by infection(presumably by heavy metal salts). The patient stated that the overalleffect of the drug was positive but complained of dizziness. Thetreatment with a C50 dilution of potentiated antibodies to thepiperidine group of IMODIUM in a dose of 1 tablet twice a day wasstarted and after five days of the therapy with antibodies theunpleasant sensations ceased (with a persisting therapeutic effect ofthe drug).

EXAMPLE 43 Potentiated Antibodies to Autologous Antigens

Potentiated antibodies to DNA antigens.

Patient P., aged 24, with clinical diagnosis of systemic lupuserythematosus accompanied by kidney affection (nephrotic typeglomerulonephritis) and heart injury (myocarditis), subacute course, IIIdegree of activity had been taking prednisolone (50 mg daily) andcurantyl (200 mg daily). Because of the lessening of the effect ofprednisolone she was began to receive potentiated polyclonal antibodiesto native DNA isolated from lymphocytes of the patients peripheralblood. Antibodies were obtained by immunization of a rabbit withsubsequent purification of the antiserum and its potentiation based onhomeopathic technology. The intake of a C1000 dilution of potentiatedantibodies to autoantigens of DNA in a dose of 1 tablet twice a dayresulted in a marked inhibition of the activity of the autoimmuneprocess within two weeks. The laboratory findings were as follows: ESRdecreased from 50 to 16 mm/h, the titer of the antinuclear factorlowered. Catamnesis: 6 months of the intake of potentiated antibodiesgave clinical and laboratory remission.

EXAMPLE 44 Potentiated Antibodies to Rhesus (Rh) Factor

Patient S., aged 28, Rh⁻ (her husband was Rh⁺) was admitted to hospitalwith the diagnosis of an 8-weeks pregnancy. This was her fourthpregnancy. She had a history of normal first pregnancy ending withnormal delivery, the second pregnancy was interrupted by medicalabortion at the term of 10 weeks, and the third pregnancy ended withantenatal death of the fetus because of the Rh conflict at the term of38 weeks. In order to prevent the Rh conflict and to maintain thecurrent pregnancy she started to take a C200 dilution of polyclonalpotentiated antibodies to Rh factor beginning with the 8th week in adose of 1 tablet twice a week. Catamnesis: the therapy favoreduncomplicated pregnancy, which ended with labor at term. The baby (Rh⁺)was healthy without symptoms of hemolytic disease.

EXAMPLE 45 Potentiated Antibodies to Substances Causing Intoxicationand/or Dependence

Potentiated antibodies to opiates.

A. Patient S., aged 28, had an almost uninterrupted 5-year history ofintravenous self-injections of crude homemade acetylated opium(sultyga). He was admitted to a narcological unit 24 hours after thelast injection. The patient was irritated and gloomy and complained ofintense pains in his extremities, chills, and insomnia. The oral intakeof 10 drops of a C200 dilution of a potentiated aqueous solution ofnatural antibodies to morphine hydrochloride every 15-30 minutes wasprescribed. The antibodies had been isolated by affinity chromatographyfrom the serum of a patient with chronic morphine dependency. Thetherapy resulted in a quick disappearance of vegetative disorders andthe lessening of the intensity of the myalgia. Six hours after thebeginning of the therapy the patient went to sleep. Two days later thewithdrawal symptoms virtually disappeared. A conclusion was drawn on thesufficiency of monotherapy with antibodies to morphine in the case ofthe opiate withdrawal syndrome.

B. Patient K., aged 21, was admitted to a narcology unit with typicalmanifestations of the opiate withdrawal syndrome. Questioning revealedthat she had been abusing crude homemade extract of poppy seed straw(koknar) in the form of intravenous self-injections in the course of twoyears. A combined therapy with a C1000 dilution of potentiatedmonoclonal antibodies to morphine in a dose of 1 tablet once in 2 hoursand a C200 dilution of potentiated antibodies to codeine in a dose of 1tablet in the morning and 1 at bedtime was prescribed. Within 48 hoursall manifestations of the withdrawal syndrome were completely arrested.

C. Patient I., aged 42, was emergently admitted to a narcology unit withthe diagnosis of codeine overdosage. The patient was somnolent and hadperiodic bouts of nausea. The examination revealed depressed reflexes,bradycardia, and moderate hypotension. The patient was put on a slowintravenous infusion of 200 ml of an isotonic solution containingpolyclonal potentiated antibodies to opiates of the phenotrene groupmixed in the following proportions: 1 ml of a C200 dilution ofantibodies to morphine; 1 ml of a C1000 dilution to codeine; 1 ml of aC50 dilution to thebaine; 1 ml of a C30 dilution to pseudomorphine; 1 mlof a C12 dilution of antibodies to neopine. Within two hours after thebeginning of the treatment the symptoms of intoxication completelydisappeared.

D. Patient D., aged 16, had been inhaling heroin at least three times aweek in the course of the last 1.5 months. On his parents' accord he washospitalized in a restricted admission unit for 24 days. Two days afteradmission he became irritable, developed sleeping disorders, andcomplained of attraction to the drug when talking to his physician. Theprescription was: a C1000 dilution of potentiated polyclonal antibodiesto HEROIN in a dose of 1 tablet 6 times a day. Three weeks later thepatient reported even mood and satisfactory sleep and appetite. Duringindividual talks with a psychologist he denied having attraction to thedrug. It was recommended to keep taking antibodies to heroin in a doseof 1 tablet a day. Two months after his discharge from hospital he(according to his mother's information) has never been noticed takingdrugs.

E. Patient Kh., aged 24, had been injecting intravenously some crudehomemade heroin preparations for three years. He was admitted to anarcology unit in a state of sopor. In view of the inefficiency ofpotentiated antibodies to heroin during his previous treatment, it wasrecommended to start the oral administration of a mixture of aqueoussolutions of monoclonal antibodies to the following synthetic andsemisynthetic opiates: a C50 dilution of antibodies to dionine(ethylmorphine); a C1000 dilution to promedol: a C30 dilution tophentanyl. Thirty minutes later the patient became fully conscious andoriented in time. His reflexes were moderately depressed. He told thephysicians that he had self-injected a dose of an unknown drug at thediscotheque.

Potentiated antibodies to barbiturates and other soporific drugs.

F. Patient B., aged 32, was admitted to an intensive care unit in thestatus epilepticus. According to his relatives, he had been takingvarious drugs of the barbiturate group both orally and intravenously inthe course of the last years. The intravenous infusion of the followingmixture of potentiated monoclonal antibodies to barbiturates wasprescribed: a C50 dilution of antibodies to barbamyl (amytal sodium); aC200 dilution to nembutal (ethaminal sodium); a C1000 dilution tofanodorm (cyclobarbital) in a dose of 1 ml each. Within 15 minutes afterthe beginning of the therapy the status epilepticus was controlled, thepatient lapsed into a stunned condition. During further observation atthe hospital the patient was irritated and suffered from insomnia anddysphoria from time to time. He tried to get hold of soporific drugs. Aninterview revealed that he had also been taking drugs of the ureidegroup (bromural) and noxyron besides barbiturates. In view of this thepatient was advised to take a C50 dilution of potentiated monoclonalantibodies to bromural in combination with a C200 dilution ofpotentiated polyclonal antibodies to noxyron 1 tablet alternately everytwo hours. The patients condition seriously improved: there was nodysphoria, he became less torpid, and his sleep was back to normal. Hestopped searching for soporific drugs and was discharged in asatisfactory condition.

Potentiated antibodies to cannabinoids.

G. Patient S., aged 24, was admitted to a psychiatric unit withpronounced depressive disorders. He had had a long history of hashishuse (up to 5-8 joints a day). As the treatment with antidepressantsproved inefficient, the oral intake of 10 ml of an aqueous solutioncontaining the following mixture of potentiated polyclonal antibodies tocannabinoids: a C50 dilution of antibodies to canabidiol; a C30 dilutionto cannabinol; a C200 dilution to (−)-trans-Δ⁹-tetrahydrocannabinol.After 10 days of the treatment the patients mood became even and hissleep was back to normal. Two weeks after the beginning of the treatmentwith anti-bodies the patient was discharged in a satisfactory condition.

H. Patient D., aged 14, had been using drugs for 6 months. She used tochew the so-called bang (hashish tar). She was willing to be treated andhis district narcologist prescribed potentiated monoclonal antibodies tocannabinoids in a dose of 1 tablet every morning according to thefollowing scheme: a C50 dilution of potentiated monoclonal antibodies toΔ⁸-tetrahydrocannabinol during the first two weeks of the month andpotentiated monoclonal antibodies to Δ⁹-tetrahydrocannabinolic acidduring the last two weeks. Six months of medical observation showed thatthe patient had given up drug abuse. The patient is socially adapted andcontinues her studies.

Potentiated antibodies to cocaine and its metabolites.

I. Patient S., aged 28, had been using crack (a mixture of cocaine withbaking soda) for 1.5 years. He was admitted to a therapeutic unit withthe diagnosis of cachexy caused by chronic hepatitis of an unknownorigin. Two weeks of health-improving therapy and hepatotropic treatmentdid not produce any significant effect. In order to control asthenicsymptoms the treatment was supplemented with tablets of a C50 dilutionof monoclonal potentiated antibodies to cocaine (in a dose of 1 tablettwice a day). After three weeks of the treatment the preparation wassubstituted by tablets containing polyclonal antibodies to cocainemetabolites: a C50 dilution of antibodies to benzoylecgonine and a C200dilution of antibodies to ecgonine. The treatment resulted in thenormalization of the patients mood and sleep; he gained 18 kg of weight.Two months after the beginning of the therapy the patient was dischargedin a satisfactory condition.

J. Patient O., aged 17, was brought to the narcological restrictedadmission unit by her parents. In the course of the last two months shehad been self-injecting cocaine solutions intravenously. An interviewwith a psychologist revealed signs of a psychic dependence on this drug.The prescription was: a C50 dilution of polyclonal antibodies to acocaine metabolite, norcocaine, in a dose of 1 tablet 3 times a dayduring the first 10 days of hospital stay. The same pattern was appliedto her second 10 days of hospital stay (a C200 dilution of polyclonalantibodies to methylecgonine) and to the third 10-days' period (a C1000dilution of polyclonal antibodies to hydroxycocaine) in the third decadeof her hospital stay. The treatment with homeopathic doses of antibodiesto cocaine metabolites resulted in a considerable improvement of thepatients condition of health: her mood became even and her sleep wasback to normal. A test before discharge one month later revealed nosigns of psychic dependence. Catamnesis four months later: the patientis socially adapted and has not been noticed using drugs.

Potentiated antibodies to benzodiazepines.

K. Patient S. aged 38, had a 20-year long history of the abuse oftranquilizers and psychotropic drugs of the benzodiazepine group.Against the background of the drug abuse the patient developed apsychoorganic syndrome with predominant astheno-apathic symptoms and thepatient was granted the 2^(nd) degree of disability. The scheme ofnootropic treatment prescribed by the district physician involved along-term intake of polyclonal potentiated antibodies to a number ofbenzodiazepines, namely, a C50 dilution of antibodies to chlozepid; aC50 dilution to diazepam; a C200 dilution to oxazepam; a C200 dilutionto nitrazepam; a C1000 dilution to lorazepam. As a result a C1000dilution of polyclonal potentiated antibodies to clonazepam proved to bethe best choice for the patient. He had been taking them every day in adose of 1 tablet twice a day for 14 months, which resulted in theimprovement of his intellectual capacities and memory. Now his behavioris well ordered; the patient is capable of taking care of himself; hismother reports that he hasn't been using any sedatives during thisperiod.

Potentiated antibodies to phenylalkylamines and other stimulants.

L. Patient C., aged 26, was admitted to a psychiatry department with thediagnosis of psychosis caused by ephedron abuse. Among the symptomsanxiety, alertness, alarming expectations, and paranoid attitudeprevailed. The intravenous administration of a C50 dilution ofpotentiated monoclonal antibodies to ephedron in a dose of 1 ml twicewithin the first hour of treatment was prescribed. After 1.5 hours ofthe therapy psychotic disorders disappeared. The patient's attitude tohis delusional episode is critical.

M. Patient Kh., aged 41, engaged at diplomatic service was admitted to aintensive care unit because of a long period (about 18 hours) ofsomnolence. According to his wife's information, the patient used toindulge alone in an intravenous administration of some stimulants butdefinitely not cocaine. The prescription was: a slow intravenousinfusion of physiological saline solution containing 1 ml of a C50dilution of potentiated antibodies to amphetamine and 1 ml a C30dilution of polyclonal potentiated antibodies to methamphetamine. Withinfifteen minutes the lethargic symptoms were arrested. The patient wasfully conscious and well oriented. He told the physician that he hadadministered a single dose of amphetamine intravenously.

N. Patient T., aged 17, administered himself ephedrine intravenouslythree times in the course of the last month for the first time in hislife. On his own initiative he went to seek for narcologist's advice, ashe was afraid of becoming an addict. The prescription was: the intake ofa combined preparation containing polyclonal antibodies to ephedrine andpolyclonal antibodies to norephedrine in a potentiated form (dilutionsC50 and C200, respectively) in a dose of 1 tablet twice a day. For halfa year the patient paid regular visits to his physician twice a monthand reported no episodes of ephedrine use during this period.

O. Patient L., aged 25, sought for narcologist's advice on his owninitiative. After 1.5 years of imprisonment he had become addicted tochifir (an extra strong tea brew) and used it at least 1-2-times a day.C50 dilution of potentiated polyclonal antibodies to caffeine(1,3,7-trimethylxanthine) in a dose of 1 tablet twice a day. During hissubsequent visits the patient stated that he had been drinking chifirvery rarely (not more often than once a week) but could not give it upaltogether.

Potentiated antibodies to hallucinogens (psychedelic drugs).

P. Patient K., aged 28, was brought to the psychiatric department from ahotel where he had attracted the hotel staffs attention by hisinadequate behavior: he was contemplating something, used to freezesuddenly and stand motionless; he was poorly oriented in the situationaround him. In response to physician's questions the patient answeredthat he used to take pieces of blotting paper impregnated with LSD,sublingually. A single dose (1 ml) of a C200 dilution of a solutioncontaining potentiated polyclonal antibodies to lysergic aciddiethylamide (LSD) was administered. Fifteen minutes after theadministration of the preparation the psychotic disorders were arrested.

Q. Two A. brothers, aged 16 and 19, with the diagnosis of poisoning withdried ink fungi were admitted to a psychiatric unit. As the quantity ofpotentiated preparation available at that moment at the unit wasinsufficient, one of the patients received intravenously 1 ml of a C200dilution of potentiated polyclonal antibodies to psilocin and the other,1 ml of a C50 dilution of potentiated polyclonal antibodies topsilocybin. Within an hour the condition of both patients returned tonormal, their excitement and unrestraint disappeared, and they both wentto sleep. A conclusion was drawn on high efficiency of bothpreparations.

R. Patient D., aged 19, was admitted to a neurology unit formanifestations of catalepsia. In view of the fact that the patient hadbeen taking the drug phenycyclidine (PCP), she underwent hourlyintramuscular administrations of 1 ml of a D3 dilution of the solutionof potentiated antibodies to phenycyclidine. Within three hours thecataleptic syndrome was completely arrested.

S. Patient A., aged 38, has the 2^(nd) degree of disability because ofparanoid schizophrenia. For fifteen years he had been taking high dailydoses of haloperidol in combination with parcopan or cyclodol for theprevention of narcolepsia and had already developed physical dependenceon them. The attending physician started reducing gradually the dose ofcyclodol ending up with replacing it completely with a C30 dilution ofpotentiated polyclonal antibodies to cyclodol in a dose of 1 tablet inthe morning and 1 tablet at bedtime every day. The patient keeps takinghaloperidol and doesn't have any neuroleptic symptoms; no requests forcyclodol prescription.

Potentiated antibodies to alkaloids of tobacco.

T. Patient I., aged 29, consulted a narcologist for tobacco smoking.Because the neuropharmacological preparations he used to take earlierhad not succeeded to rid him of the bad habit, the physician prescribeda C200 dilution of a potentiated antiserum to nicotine in a dose of 1tablet 3 times a day. Catamnesis 3 months later was as follows: in thecourse of the first weeks of the therapy with antibodies the patient'scraving for tobacco was enhanced and he smoked more often. Later on, thesituation changed, his craving receded, he was able to gradually reducethe number of smoked cigarettes and finally to give up smokingaltogether.

Potentiated antibodies to alcohol.

U. Patient B., aged 35, was admitted to a narcological hospital withpronounced symptoms of alcohol withdrawal. A C200 dilution ofpotentiated monoclonal antibodies to ethanol in a dose of 1 sublingualtablet every 15 minutes was prescribed. Within two hours of the therapythe patients condition significantly improved: the tremor,hyperhydrosis, and weakness disappeared, the patient went to sleep.Twenty-four hours later he was discharged. Conclusion: potentiatedantibodies to ethanol have a therapeutic effect in the case of thealcohol withdrawal syndrome.

EXAMPLE 46 Potentiated Antibodies to Antigens of Fetal and PrimordialTissues and Tissue Cultures

A. Patient A. was a newborn baby 27 days old. He was born with symptomsof perinatal encephalopathy. As immunoenzyme diagnostic methods hadrevealed elevated levels of embryotropic neurospecific antigens inmother before this pregnancy, it was decided to administer to the baby aC200 dilution of a potentiated polyclonal antiserum to bovine fetalbrain-specific non-species-specific protein (antigen), 14-3-2(brain-specific enolase), in an oral dose of 5 drops of an aqueoussolution to be administered 3 times a day. In the course of thetreatment neurological symptoms subsided gradually; the reflexes of oraland spinal automatism restored and muscle hypertonus receded. The babybecame calmer and started active breast sucking. A conclusion was drawnon the efficiency of potentiated antibodies to the said fetal antigencontrolling normal morphogenesis of the central nervous system in thetreatment of perinatal encephalopathy.

B. Patient D., aged 4, with an established diagnosis of mentalretardation had been receiving a C1000 dilution of monoclonalpotentiated antibodies to primordial antigen nestin, a protein marker ofneuron stem cells, in a dose of 5 drops of an aqueous solution once aday in the morning for six months with the purpose of enhancing thechild's intellectual capacities. After six months of the treatment aneuropsychological examination showed that D's intellect and memory wereup to the standard age level; the child's kindergarten tutor reportedthat the boy comprehended and learned the material well in class.

C. Patient I., aged 8, with an established diagnosis of Down's syndromehad been receiving a C200 dilution of potentiated polyclonal antibodiesto A-fetoprotein to be taken in a dose of 1 tablet a day for the first12 months and in a dose of 1 tablet once in 3 days for subsequent 6months. The neuropsychological examination by Bailey's method revealed amarked enhancement of the patient's intellect 1.5 years later. Thepatient's behavior is well ordered; he is adapted to being with otherchildren.

D. Patient S., aged 18, suffered from myasthenia of an unknown origin.In view of the inefficiency of conventional drugs the treatment wassupplemented by the oral intake of a C30 dilution of potentiatedpolyclonal antibodies to the culture of neuronal stem cell of the tera-1line enriched with the protein extract of the embryonic tissue in a doseof 1 ml 3 times a day for 6 months. The combined treatment resulted inan increased tolerance of physical strain, receded bulbar symptoms,diplopia, and ptosis, which made it possible to reduce the daily dosesof corticosteroid drugs several times.

E. Patient M., aged 42, suffered from the astheno-neurological syndromeaccompanying the remote period of vernal encephalitis. As conventionaltherapy proved its inefficiency, it was decided to prescribe the oralintake of a C200 dilution of potentiated polyclonal antibodies toembryonic neocortex (the antiserum was obtained by immunization ofrabbits with tissues from the occipital zone of the brain cortex of15-day old embryos of Wistar line rats) in a dose of 1 ml twice a day,for 6 months. In the course of treatment the patient's asthenic symptomsbecame less pronounced, his ability to work was restored, thoughdisseminated microsymptoms persisted in his neurological status.

F. Patient K., aged 39, suffered from chronic alcoholism, grade II. Hewent to seek for narcologist's advice declaring his desire to start asober life and asking for a new method of treatment because those he hadalready tried were of little effect. The prescription was: a regularintake of a C1000 dilution of polyclonal potentiated antibodies tohomogenized hippocampi of embryos of Wistar line rats (hippocampi ofseveral dozens of syngenic fetuses were used for immunization) in a doseof 1 tablet once a day. The remission had been lasting for 8 months, inthe course of this period of medical observation no episodes ofconsuming alcoholic beverages have been registered, the patient statesthe absence of craving for alcohol.

G. Patient A., aged 8, suffered from liver cirrhosis of an unknownetiology. As the conventional therapy had no significant effect, theoral intake of a C4 dilution of polyclonal potentiated antibodies tohomogenized liver of the human fetus was prescribed in a dose of 1 ml 3times a day. During four months of the therapy a clinical improvement ofthe patient's condition was observed, manifestations of generalintoxication symptoms and liver failure subsided. The patients emotionaltone rose, the paleness of skin, the icteric hue of the scleras, andspider-like hemangiomas disappeared; the size of the liver diminished. Aconclusion was drawn on high efficiency of this mode of treatment.

EXAMPLE 47 Potentiated Antibodies to Tissues or Tissue Cultures

A. Patient O., aged 8, suffers from a malignant course ofinsulin-dependent diabetes mellitus. The intranasal administration of aC50 dilution of potentiated polyclonal antibodies to a culture ofinsular cells of the pancreas of newborn rabbits in a dose of 1 ml 3times a day was prescribed with therapeutic purposes. After three monthsof the therapy the course of illness became stable, the blood glucoselevel went down, and the disposition to ketoacidosis receded. There wereno comas or hypoglycemic episodes during the period of the treatment andthe amount of insulin intake was reduced by 50%.

B. Patient P., aged 35, suffered from insulin-dependent diabetesmellitus (mild course). As the patient was unwilling to take insulin,the recommendation was to start the oral intake of 1 ml of a C50dilution of an aqueous solution of polyclonal potentiated antiserum toinsular cells of the pancreas of a newborn calf once a day. As a resultof the monotherapy with this preparation, the patient was feeling well.Her blood glucose level was within normal limits. The patient did nottake insulin any more.

C. Patient V. aged 56, suffered from obstructing atherosclerosis ofcoronary arteries and angina decubitus. In view the inefficiency ofconventional therapy the prescription was to take intranasally a C30dilution of potentiated polyclonal antibodies to the homogenized heartof a newborn rabbit in a dose of 3 drops of an aqueous solution 5 timesa day. After six months of the therapy the intensity of pain wasreduced, the patient had pain much more seldom and only after asufficiently strong physical strain; his blood lipid formula becamenormal and the dose of nitrate drugs was reduced approximately by 50%.

Thus, an analysis of the examples given above shows that the activatedform of ultra-low doses of antibodies to an antigen (a substance or apharmaceutical agent) does not produce the well-known immunologicaleffect of binding the antigen and inhibiting its activity; on thecontrary, it reproduces the antigen's activity in a modified form, whichresults in a partial or complete reduction of the pathological syndrome,in the regulation of whose mechanisms of development said antigen isinvolved. In this case such antigen-associated side effects as toxicity,addiction, and tolerance are absent.

In addition, activated antibodies in ultra-low doses potentiate(reinforce) the effect of an antigen (a pharmaceutical agent) on theircombined or simultaneous administration, which makes it possible toreduce the dose of the pharmaceutical agent and to minimize its sideeffects.

The administration of activated forms of ultra-low doses of antibodiesto a substance or a pharmaceutical agent favors the reduction of theintensity of the pathological syndromes (acute or chronic intoxication,post-intoxication disorders, dependence) caused by this substance orpharmaceutical agent.

Experimental studies of activated forms of ultra-low doses of antibodiesmake it possible to determine their therapeutic properties even insituations where the biological activity of the initial antigen remainsunknown.

The invention claimed is:
 1. A method of administering to a subjectsuffering from sleep disorder a homeopathically activated form of anantibody to a pharmaceutical agent, wherein the molecular form of saidpharmaceutical agent is involved in the regulation of said sleepdisorder.
 2. The method of claim 1 wherein said pharmaceutical agent isselected from zopiclone, midazolam, nitrazepam, zolpidem, diazepam, andamitriptyline.